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学者姓名:武淑芳

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Defective autophagy in osteoblasts induces endoplasmic reticulum stress and causes remarkable bone loss SCIE PubMed Scopus
期刊论文 | 2018 , 14 (10) , 1726-1741 | AUTOPHAGY
SCOPUS Cited Count: 1
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Abstract :

Macroautophagy/autophagy is a highly regulated process involved in the turnover of cytosolic components, however its pivotal role in maintenance of bone homeostasis remains elusive. In the present study, we investigated the direct role of ATG7 (autophagy related 7) during developmental and remodeling stages in vivo using osteoblast-specific Atg7 conditional knockout (cKO) mice. Atg7 cKO mice exhibited a reduced bone mass at both developmental and adult age. The trabecular bone volume of Atg7 cKO mice was significantly lower than that of controls at 5 months of age. This phenotype was attributed to decreased osteoblast formation and matrix mineralization, accompanied with an increased osteoclast number and the extent of the bone surface covered by osteoclasts as well as an elevated secretion of TNFSF11/RANKL (tumor necrosis factor [ligand] superfamily, member 11), and a decrease in TNFRSF11B/OPG (tumor necrosis factor receptor superfamily, member 11b [osteoprotegerin]). Remarkably, Atg7 deficiency in osteoblasts triggered endoplasmic reticulum (ER) stress, whereas attenuation of ER stress by administration of phenylbutyric acid in vivo abrogated Atg7 ablation-mediated effects on osteoblast differentiation, mineralization capacity and bone formation. Consistently, Atg7 deficiency impeded osteoblast mineralization and promoted apoptosis partially in DDIT3/CHOP (DNA-damage-inducible transcript 3)- and MAPK8/JNK1 (mitogen-activated protein kinase 8)-SMAD1/5/8-dependent manner in vitro, while reconstitution of Atg7 could improve ER stress and restore skeletal balance. In conclusion, our findings provide direct evidences that autophagy plays crucial roles in regulation of bone homeostasis and suggest an innovative therapeutic strategy against skeletal diseases.

Keyword :

osteoporosis bone mass bone formation ER stress Autophagy

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GB/T 7714 Li, Huixia , Li, Danhui , Ma, Zhengmin et al. Defective autophagy in osteoblasts induces endoplasmic reticulum stress and causes remarkable bone loss [J]. | AUTOPHAGY , 2018 , 14 (10) : 1726-1741 .
MLA Li, Huixia et al. "Defective autophagy in osteoblasts induces endoplasmic reticulum stress and causes remarkable bone loss" . | AUTOPHAGY 14 . 10 (2018) : 1726-1741 .
APA Li, Huixia , Li, Danhui , Ma, Zhengmin , Qian, Zhuang , Kang, Xiaomin , Jin, Xinxin et al. Defective autophagy in osteoblasts induces endoplasmic reticulum stress and causes remarkable bone loss . | AUTOPHAGY , 2018 , 14 (10) , 1726-1741 .
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Sirtuin-1 (SIRT1) stimulates growth-plate chondrogenesis by attenuating the PERK-eIF-2-CHOP pathway in the unfolded protein response EI SCIE PubMed Scopus
期刊论文 | 2018 , 293 (22) , 8614-8625 | JOURNAL OF BIOLOGICAL CHEMISTRY
WoS CC Cited Count: 2 SCOPUS Cited Count: 2
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Abstract :

The NAD(+)-dependent deacetylase sirtuin-1 (SIRT1) has emerged as an important regulator of chondrogenesis and cartilage homeostasis, processes that are important for physiological skeletal growth and that are dysregulated in osteoarthritis. However, the functional role and underlying mechanism by which SIRT1 regulates chondrogenesis remain unclear. Using cultured rat metatarsal bones and chondrocytes isolated from rat metatarsal rudiments, here we studied the effects of the SIRT1 inhibitor EX527 or of SIRT1 siRNA on chondrocyte proliferation, hypertrophy, and apoptosis. We show that EX527 or SIRT1 siRNA inhibits chondrocyte proliferation and hypertrophy and induces apoptosis. We also observed that SIRT1 inhibition mainly induces the PERK-eIF-2-CHOP axis of the endoplasmic reticulum (ER) stress response in growth-plate chondrocytes. Of note, EX527- or SIRT1 siRNA-mediated inhibition of metatarsal growth and growth-plate chondrogenesis were partly neutralized by phenylbutyric acid, a chemical chaperone that attenuates ER stress. Moreover, EX527-mediated impairment of chondrocyte function (i.e. of chondrocyte proliferation, hypertrophy, and apoptosis) was partly reversed in CHOP-/- cells. We also present evidence that SIRT1 physically interacts with and deacetylates PERK. Collectively, our findings indicate that SIRT1 deacetylates PERK and attenuates the PERK-eIF-2-CHOP axis of the unfolded protein response pathway and thereby promotes growth-plate chondrogenesis and longitudinal bone growth.

Keyword :

bone growth chondrocyte PERK unfolded protein response (UPR) chondrogenesis sirtuin 1 (SIRT1) growth plate endoplasmic reticulum stress (ER stress)

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GB/T 7714 Kang, Xiaomin , Yang, Wei , Wang, Ruiqi et al. Sirtuin-1 (SIRT1) stimulates growth-plate chondrogenesis by attenuating the PERK-eIF-2-CHOP pathway in the unfolded protein response [J]. | JOURNAL OF BIOLOGICAL CHEMISTRY , 2018 , 293 (22) : 8614-8625 .
MLA Kang, Xiaomin et al. "Sirtuin-1 (SIRT1) stimulates growth-plate chondrogenesis by attenuating the PERK-eIF-2-CHOP pathway in the unfolded protein response" . | JOURNAL OF BIOLOGICAL CHEMISTRY 293 . 22 (2018) : 8614-8625 .
APA Kang, Xiaomin , Yang, Wei , Wang, Ruiqi , Xie, Tianping , Li, Huixia , Feng, Dongxu et al. Sirtuin-1 (SIRT1) stimulates growth-plate chondrogenesis by attenuating the PERK-eIF-2-CHOP pathway in the unfolded protein response . | JOURNAL OF BIOLOGICAL CHEMISTRY , 2018 , 293 (22) , 8614-8625 .
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Melatonin protects chondrocytes from impairment induced by glucocorticoids via NAD(+)-dependent SIRT1 SCIE PubMed Scopus
期刊论文 | 2017 , 126 , 24-29 | STEROIDS | IF: 2.523
WoS CC Cited Count: 1
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Abstract :

Intra-articular injection of glucocorticoids is used to relieve pain and inflammation in osteoarthritis patients, which is occasionally accompanied with the serious side effects of glucocorticoids in collagen-producing tissue. Melatonin is the major hormone released from the pineal gland and its beneficial effects: on cartilage has been suggested. In the present study, we investigated the protective role of melatonin on matrix degeneration in chondrocytes induced by dexamethasone (Dex). The chondrocytes isolated from mice knee joint were treated with Dex, melatonin, EX527 and siRNA targeted for SIRT6, respectively. Dex treatment induced the loss of the extracellular matrix, NAD(+)/NADH ratio and NADPH concentration in chondrocytes. Melatonin alone have no effect on the quantity of proteoglycans and collagen type Hal, however, the pretreatment of melatonin reversed the negative effects induced by Dex. Meanwhile, the significant decrease in NAD(+)/NADH ratio and NADPH concentration in Dex group were up-regulated by pretreatment of melatonin. Furthermore, it was revealed that inhibition of SIRT1 blocked the protective effects of melatonin. The enhancement of NAD(+)-dependent SIRT1 activity contributes to the chondroprotecfive effects of melatonin, which has a great benefit to prevent dexamethasone-induced chondrocytes impairment.

Keyword :

SIRT1 Osteoarthritis Glucocorticoids NAD(+) Melatonin Chondrocytes

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GB/T 7714 Yang, Wei , Kang, Xiaomin , Qin, Na et al. Melatonin protects chondrocytes from impairment induced by glucocorticoids via NAD(+)-dependent SIRT1 [J]. | STEROIDS , 2017 , 126 : 24-29 .
MLA Yang, Wei et al. "Melatonin protects chondrocytes from impairment induced by glucocorticoids via NAD(+)-dependent SIRT1" . | STEROIDS 126 (2017) : 24-29 .
APA Yang, Wei , Kang, Xiaomin , Qin, Na , Li, Feng , Jin, Xinxin , Ma, Zhengmin et al. Melatonin protects chondrocytes from impairment induced by glucocorticoids via NAD(+)-dependent SIRT1 . | STEROIDS , 2017 , 126 , 24-29 .
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Cartilage-Specific Autophagy Deficiency Promotes ER Stress and Impairs Chondrogenesis in PERK-ATF4-CHOP-Dependent Manner SCIE PubMed
期刊论文 | 2017 , 32 (10) , 2128-2141 | JOURNAL OF BONE AND MINERAL RESEARCH | IF: 6.314
WoS CC Cited Count: 6
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Abstract :

Autophagy is activated during nutritionally depleted or hypoxic conditions to facilitate cell survival. Because growth plate is an avascular and hypoxic tissue, autophagy may have a crucial role during chondrogenesis; however, the functional role and underlying mechanism of autophagy in regulation of growth plate remains elusive. In this study, we generated (TamCart)Atg7(-/-) (Atg7cKO) mice to explore the role of autophagy during endochondral ossification. Atg7cKO mice exhibited growth retardation associated with reduced chondrocyte proliferation and differentiation, and increased chondrocyte apoptosis. Meanwhile, we observed that Atg7 ablation mainly induced the PERK-ATF4-CHOP axis of the endoplasmic reticulum (ER) stress response in growth plate chondrocytes. Although Atg7 ablation induced ER stress in growth plate chondrocytes, the addition of phenylbutyric acid (PBA), a chemical chaperone known to attenuate ER stress, partly neutralized such effects of Atg7 ablation on longitudinal bone growth, indicating the causative interaction between autophagy and ER stress in growth plate. Consistent with these findings in vivo, we also observed that Atg7 ablation in cultured chondrocytes resulted in defective autophagy, elevated ER stress, decreased chondrocytes proliferation, impaired expression of col10a1, MMP13, and VEGFA for chondrocyte differentiation, and increased chondrocyte apoptosis, while such effects were partly nullified by reduction of ER stress with PBA. In addition, Atg7 ablation-mediated impaired chondrocyte function (chondrocyte proliferation, differentiation, and apoptosis) was partly reversed in CHOP-/- cells, indicating the causative role of the PERK-ATF4-CHOP axis of the ER stress response in the action of autophagy deficiency in chondrocytes. In conclusion, our findings indicate that autophagy deficiency may trigger ER stress in growth plate chondrocytes and contribute to growth retardation, thus implicating autophagy as an important regulator during chondrogenesis and providing new insights into the clinical potential of autophagy in cartilage homeostasis. (C) 2017 American Society for Bone and Mineral Research.

Keyword :

ENDOCHONDRAL OSSIFICATION GROWTH PLATE CHONDROCYTES ATG7 ER STRESS AUTOPHAGY

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GB/T 7714 Kang, Xiaomin , Yang, Wei , Feng, Dongxu et al. Cartilage-Specific Autophagy Deficiency Promotes ER Stress and Impairs Chondrogenesis in PERK-ATF4-CHOP-Dependent Manner [J]. | JOURNAL OF BONE AND MINERAL RESEARCH , 2017 , 32 (10) : 2128-2141 .
MLA Kang, Xiaomin et al. "Cartilage-Specific Autophagy Deficiency Promotes ER Stress and Impairs Chondrogenesis in PERK-ATF4-CHOP-Dependent Manner" . | JOURNAL OF BONE AND MINERAL RESEARCH 32 . 10 (2017) : 2128-2141 .
APA Kang, Xiaomin , Yang, Wei , Feng, Dongxu , Jin, Xinxin , Ma, Zhengmin , Qian, Zhuang et al. Cartilage-Specific Autophagy Deficiency Promotes ER Stress and Impairs Chondrogenesis in PERK-ATF4-CHOP-Dependent Manner . | JOURNAL OF BONE AND MINERAL RESEARCH , 2017 , 32 (10) , 2128-2141 .
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Local intra-articular injection of resveratrol delays cartilage degeneration in C57BL/6 mice by inducing autophagy via AMPK/mTOR pathway SCIE PubMed Scopus
期刊论文 | 2017 , 134 (3) , 166-174 | JOURNAL OF PHARMACOLOGICAL SCIENCES | IF: 2.575
WoS CC Cited Count: 6
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Abstract :

Autophagy is an essential cellular homeostasis mechanism that was found to be compromised in aging and osteoarthritis (OA) cartilage. Previous studies showed that resveratrol can effectively regulate autophagy in other cells. The purpose of this study was to determine whether the chondroprotective effect of resveratrol was related to chondrocyte autophagy and to elucidate underlying mechanisms. OA model was induced by destabilization of the medial meniscus (DMM) in 10-week-old male mice. OA mice were treated with resveratrol with/without 3-MA for 8 weeks beginning 4 weeks after surgery. The local intra-articular injection of resveratrol delayed articular cartilage degradation in DMM-induced OA by OARSI scoring systems and Safranin O-fast green. Resveratrol treatment increased Unc-51-like kinase1, Beclin1, microtubule-associated protein light chain 3, hypoxia inducible factor-1 alpha, phosphorylated AMPK, collagen-2A1, Aggrecan expressions, but decreased hypoxia inducible factor-2 alpha, phosphorylated mTOR, matrix metalloproteinases13 and a disintegrin and metalloproteinase with thrombospondin motifs 5 expressions. The effects of resveratrol were obviously blunted by 3-MA except HIF and AMPK. These findings indicate that resveratrol intra-articular injection delayed articular cartilage degeneration and promoted chondrocyte autophagy in an experimental model of surgical DMM-induced OA, in part via balancing HIF-1 alpha and HIF-2 alpha expressions and thereby regulating AMPK/mTOR signaling pathway. (C) 2017 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society.

Keyword :

Mammalian target of rapamycin Resveratrol AMP activated protein kinase Osteoarthritis Autophagy

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GB/T 7714 Qin, Na , Wei, Liwei , Li, Wuyin et al. Local intra-articular injection of resveratrol delays cartilage degeneration in C57BL/6 mice by inducing autophagy via AMPK/mTOR pathway [J]. | JOURNAL OF PHARMACOLOGICAL SCIENCES , 2017 , 134 (3) : 166-174 .
MLA Qin, Na et al. "Local intra-articular injection of resveratrol delays cartilage degeneration in C57BL/6 mice by inducing autophagy via AMPK/mTOR pathway" . | JOURNAL OF PHARMACOLOGICAL SCIENCES 134 . 3 (2017) : 166-174 .
APA Qin, Na , Wei, Liwei , Li, Wuyin , Yang, Wei , Cai, Litao , Qian, Zhuang et al. Local intra-articular injection of resveratrol delays cartilage degeneration in C57BL/6 mice by inducing autophagy via AMPK/mTOR pathway . | JOURNAL OF PHARMACOLOGICAL SCIENCES , 2017 , 134 (3) , 166-174 .
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Clock Gene Bmal1 Modulates Human Cartilage Gene Expression by Crosstalk With Sirt1 SCIE PubMed Scopus
期刊论文 | 2016 , 157 (8) , 3096-3107 | ENDOCRINOLOGY | IF: 4.286
WoS CC Cited Count: 10
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Abstract :

The critical regulation of the peripheral circadian gene implicated in osteoarthritis (OA) has been recently recognized; however, the causative role and clinical potential of the peripheral circadian rhythm attributable to such effects remain elusive. The purpose of this study was to elucidate the role of a circadian gene Bmal1 in human cartilage and pathophysiology of osteoarthritis. In our present study, the mRNA and protein levels of circadian rhythm genes, including nicotinamide adenine dinucleotide oxidase (NAD beta) and sirtuin 1 (Sirt1), in human knee articular cartilage were determined. In OA cartilage, the levels of both Bmal1 and NAD beta decreased significantly, which resulted in the inhibition of nicotinamide phosphoribosyltransferase activity and Sirt1 expression. Furthermore, the knockdown of Bmal1 was sufficient to decrease the level of NAD beta and aggravate OA-like gene expression changes under the stimulation of IL-1 beta. The overexpression of Bmal1 relieved the alteration induced by IL-1 beta, which was consistent with the effect of the inhibition of Rev-Erb beta (known as NR1D1, nuclear receptor subfamily 1, group D). On the other hand, the trans-fection of Sirt1 small interfering RNA not only resulted in a reduction of the protein expression of Bmal1 and a moderate increase of period 2 (per2) and Rev-Erb alpha but also further exacerbated the survival of cells and the expression of cartilage matrix-degrading enzymes induced by IL-1 beta. Overexpression of Sirt1 restored the metabolic imbalance of chondrocytes caused by IL-1 beta. These observations suggest that Bmal1 is a key clock gene to involve in cartilage homeostasis mediated through sirt1 and that manipulating circadian rhythm gene expression implicates an innovative strategy to develop novel therapeutic agents against cartilage diseases.

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GB/T 7714 Yang, Wei , Kang, Xiaomin , Liu, Jiali et al. Clock Gene Bmal1 Modulates Human Cartilage Gene Expression by Crosstalk With Sirt1 [J]. | ENDOCRINOLOGY , 2016 , 157 (8) : 3096-3107 .
MLA Yang, Wei et al. "Clock Gene Bmal1 Modulates Human Cartilage Gene Expression by Crosstalk With Sirt1" . | ENDOCRINOLOGY 157 . 8 (2016) : 3096-3107 .
APA Yang, Wei , Kang, Xiaomin , Liu, Jiali , Li, Huixia , Ma, Zhengmin , Jin, Xinxin et al. Clock Gene Bmal1 Modulates Human Cartilage Gene Expression by Crosstalk With Sirt1 . | ENDOCRINOLOGY , 2016 , 157 (8) , 3096-3107 .
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Bilaterally Primary Cementless Total Hip Arthroplasty for Severe Hip Ankylosis with Ankylosing Spondylitis SCIE PubMed
期刊论文 | 2016 , 8 (3) , 352-359 | ORTHOPAEDIC SURGERY | IF: 1.237
WoS CC Cited Count: 2
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ObjectivesTotal hip arthroplasty is a reliable therapeutic intervention in patients with ankylosing spondylitis, in whom the aims of surgery are to reduce pain, restore hip function and improve quality of life. The current study is a retrospective analysis of the clinical and radiographic findings in a consecutive series of patients with hip ankylosis associated with severe ankylosing spondylitis who underwent bilateral primary total hip arthroplasty using non-cemented components. MethodsFrom June 2008 to May 2012, total hip arthroplasty was performed on 34 hips in 17 patients with bilateral ankylosis caused by ankylosing spondylitis. The study patients included 13 men and 4 women with a mean age of 24.2 years. The mean duration of disease was 8.3 years and the average duration of hip involvement was 7.6 years. All patients had severe hip pain and dysfunction with bilateral bony ankylosis and no range of motion preoperatively and all underwent bilateral cementless total hip arthroplasty performed by a single surgeon. Joint pain, range of motion (ROM), and Harris hip scores were assessed to evaluate the postoperative results. ResultsAt a mean follow-up of 31.7 months, all patients had experienced significant clinical improvement in function, ROM, posture and ambulation. At the final follow-up, the mean postoperative flexion ROM was 134.4 degrees compared with 0 degrees preoperatively. Similar improvements were seen in hip abduction, adduction, internal rotation and external rotation. Postoperatively, 23 hips were completely pain-free, six had only occasional discomfort, three mild to moderate pain and two severe pain. The average Harris Hip Score improved from 23.7 preoperatively to 65.8 postoperatively. No stems had loosened at the final follow-up in any patient, nor had any revision surgery been required. ConclusionsBilateral severe hip ankylosis in patients with ankylosing spondylitis can be treated with cementless bilateral synchronous total hip arthroplasty, which can greatly improve hip joint function and relieve pain without significant complications. Provided the overall physical condition of a patient and their economic situation make surgery a feasible option and the surgeon is experienced, this treatment is a worthwhile surgical intervention for bilateral hip bony ankylosis. However, the technically demanding nature of the procedure and potential pre- and post-operative problems should not be underestimated.

Keyword :

Total hip arthroplasty Ankylosing spondylitis Non-cemented

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GB/T 7714 Feng, Dong-xu , Zhang, Kun , Zhang, Yu-min et al. Bilaterally Primary Cementless Total Hip Arthroplasty for Severe Hip Ankylosis with Ankylosing Spondylitis [J]. | ORTHOPAEDIC SURGERY , 2016 , 8 (3) : 352-359 .
MLA Feng, Dong-xu et al. "Bilaterally Primary Cementless Total Hip Arthroplasty for Severe Hip Ankylosis with Ankylosing Spondylitis" . | ORTHOPAEDIC SURGERY 8 . 3 (2016) : 352-359 .
APA Feng, Dong-xu , Zhang, Kun , Zhang, Yu-min , Nian, Yue-wen , Zhang, Jun , Kang, Xiao-min et al. Bilaterally Primary Cementless Total Hip Arthroplasty for Severe Hip Ankylosis with Ankylosing Spondylitis . | ORTHOPAEDIC SURGERY , 2016 , 8 (3) , 352-359 .
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Total ginsenosides suppress monocrotaline-induced pulmonary hypertension in rats: involvement of nitric oxide and mitogen-activated protein kinase pathways SCIE PubMed Scopus
期刊论文 | 2016 , 40 (3) , 285-291 | JOURNAL OF GINSENG RESEARCH | IF: 4.082
WoS CC Cited Count: 3 SCOPUS Cited Count: 2
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Background: Ginsenosides have been shown to exert beneficial pharmacological effects on the central nervous, cardiovascular, and endocrine systems. We sought to determine whether total ginsenosides (TG) inhibit monocrotaline (MCT)-induced pulmonary hypertension and to elucidate the underlying mechanism. Methods: MCT-intoxicated rats were treated with gradient doses of TG, with or without NG-nitro-Larginine methyl ester. The levels of molecules involving the regulation of nitric oxide and mitogen-activated protein kinase pathways were determined. Results: TG ameliorated MCT-induced pulmonary hypertension in a dose-dependent manner, as assessed by the right ventricular systolic pressure, the right ventricular hypertrophy index, and pulmonary arterial remodeling. Furthermore, TG increased the levels of pulmonary nitric oxide, endothelial nitric oxide synthase, and cyclic guanosine monophosphate. Lastly, TG increased mitogen-activated protein kinase phosphatase-1 expression and promoted the dephosphorylation of extracellular signal-regulated protein kinases 1/2, p38 mitogen-activated protein kinase, and c-Jun NH2-terminal kinase 1/2. Conclusion: TG attenuates MCT-induced pulmonary hypertension, which may involve in part the regulation of nitric oxide and mitogen-activated protein kinase pathways. Copyright (C) 2015, The Korean Society of Ginseng, Published by Elsevier.

Keyword :

endothelial nitric oxide synthase nitric oxide pulmonary hypertension total ginsenoside mitogen-activated protein kinases

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GB/T 7714 Qin, Na , Yang, Wei , Feng, Dongxu et al. Total ginsenosides suppress monocrotaline-induced pulmonary hypertension in rats: involvement of nitric oxide and mitogen-activated protein kinase pathways [J]. | JOURNAL OF GINSENG RESEARCH , 2016 , 40 (3) : 285-291 .
MLA Qin, Na et al. "Total ginsenosides suppress monocrotaline-induced pulmonary hypertension in rats: involvement of nitric oxide and mitogen-activated protein kinase pathways" . | JOURNAL OF GINSENG RESEARCH 40 . 3 (2016) : 285-291 .
APA Qin, Na , Yang, Wei , Feng, Dongxu , Wang, Xinwen , Qi, Muyao , Du, Tianxin et al. Total ginsenosides suppress monocrotaline-induced pulmonary hypertension in rats: involvement of nitric oxide and mitogen-activated protein kinase pathways . | JOURNAL OF GINSENG RESEARCH , 2016 , 40 (3) , 285-291 .
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Progranulin induces adipose insulin resistance and autophagic imbalance via TNFR1 in mice SCIE PubMed
期刊论文 | 2015 , 55 (3) , 231-243 | JOURNAL OF MOLECULAR ENDOCRINOLOGY | IF: 2.947
WoS CC Cited Count: 11
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Progranulin (PGRN) has recently emerged as an important regulator for insulin resistance. However, the direct effect of PGRN in vivo and the underlying role of progranulin in adipose insulin resistance involving the autophagy mechanism is not fully understood. In this study, mice treated with PGRN for 21 days exhibited the impaired glucose tolerance and insulin sensitivity, remarkable adipose autophagy as well as attenuated insulin signaling via inhibition of mammalian target of rapamycin (mTOR) pathway. Furthermore, blockade of tumor necrosis factor receptor 1 (TNFR1) by TNFR1BP-Fc injection resulted in the restoration of impaired insulin sensitivity and insulin signaling induced by PGRN. Consistent with these findings in vivo, PGRN treatment induced defective insulin signaling, abnormal autophagic and mitochondrial activity in cultured adipocytes, while such effects were nullified by the blockade of TNFR1. In addition, PGRN-deficient adipocytes were more refractory to tunicamycin-or dexamethasone-induced insulin resistance, indicating the causative role of the TNFR1 pathway in the action of PGRN. Collectively, our findings support the notion that PGRN is a key regulator of insulin resistance and that PGRN may mediate its effects, at least in part, by inducing autophagy via the TNFR1-dependent mechanism.

Keyword :

TNFR1 progranulin adipocytes insulin resistance autophagy

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GB/T 7714 Zhou, Bo , Li, Huixia , Liu, Jiali et al. Progranulin induces adipose insulin resistance and autophagic imbalance via TNFR1 in mice [J]. | JOURNAL OF MOLECULAR ENDOCRINOLOGY , 2015 , 55 (3) : 231-243 .
MLA Zhou, Bo et al. "Progranulin induces adipose insulin resistance and autophagic imbalance via TNFR1 in mice" . | JOURNAL OF MOLECULAR ENDOCRINOLOGY 55 . 3 (2015) : 231-243 .
APA Zhou, Bo , Li, Huixia , Liu, Jiali , Xu, Lin , Guo, Qinyue , Sun, Hongzhi et al. Progranulin induces adipose insulin resistance and autophagic imbalance via TNFR1 in mice . | JOURNAL OF MOLECULAR ENDOCRINOLOGY , 2015 , 55 (3) , 231-243 .
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PGRN Induces Impaired Insulin Sensitivity and Defective Autophagy in Hepatic Insulin Resistance SCIE PubMed Scopus
期刊论文 | 2015 , 29 (4) , 528-541 | MOLECULAR ENDOCRINOLOGY | IF: 3.432
WoS CC Cited Count: 13 SCOPUS Cited Count: 14
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Progranulin (PGRN) has recently emerged as an important regulator for glucose metabolism and insulin sensitivity. However, the underlying mechanisms of PGRN in the regulation of insulin sensitivity and autophagy remain elusive. In this study, we aimed to address the direct effects of PGRN in vivo and to evaluate the potential interaction of impaired insulin sensitivity and autophagic disorders in hepatic insulin resistance. We found that mice treated with PGRN for 21 days exhibited the impaired glucose tolerance and insulin tolerance and hepatic autophagy imbalance as well as defective insulin signaling. Furthermore, treatment of mice with TNF receptor (TNFR)-1 blocking peptide-Fc, a TNFR1 blocking peptide-Fc fusion protein to competitively block the interaction of PGRN and TNFR1, resulted in the restoration of systemic insulin sensitivity and the recovery of autophagy and insulin signaling in liver. Consistent with these findings in vivo, we also observed that PGRN treatment induced defective autophagy and impaired insulin signaling in hepatocytes, with such effects being drastically nullified by the addition of TNFR1 blocking peptide -Fc or TNFR1-small interference RNA via the TNFR1-nuclear factor-kappa B-dependent manner, indicating the causative role of PGRN in hepatic insulin resistance. In conclusion, our findings supported the notion that PGRN is a key regulator of hepatic insulin resistance and that PGRN may mediate its effects, at least in part, by inducing defective autophagy via TNFR1/nuclear factor-kappa B.

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GB/T 7714 Liu, Jiali , Li, Huixia , Zhou, Bo et al. PGRN Induces Impaired Insulin Sensitivity and Defective Autophagy in Hepatic Insulin Resistance [J]. | MOLECULAR ENDOCRINOLOGY , 2015 , 29 (4) : 528-541 .
MLA Liu, Jiali et al. "PGRN Induces Impaired Insulin Sensitivity and Defective Autophagy in Hepatic Insulin Resistance" . | MOLECULAR ENDOCRINOLOGY 29 . 4 (2015) : 528-541 .
APA Liu, Jiali , Li, Huixia , Zhou, Bo , Xu, Lin , Kang, Xiaomin , Yang, Wei et al. PGRN Induces Impaired Insulin Sensitivity and Defective Autophagy in Hepatic Insulin Resistance . | MOLECULAR ENDOCRINOLOGY , 2015 , 29 (4) , 528-541 .
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