Down-regulation of programmed cell death 5 by insulin-like growth factor 1 in osteoarthritis chondrocytes

Che, Yi; Ma, Chunhui; Xie, Zongping; Zhang, Guoqiao; Song, Wei; Zhou, Xiaokai; Cao, Yun

doi:10.1007/s00264-012-1744-x

Cited by 15 publications

(9 citation statements)

References 33 publications

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“…Immunohistochemical analysis for IGF-1 expression was chosen because myocardial IGF-1 expression was considered to be the most relevant parameter in the physiopathology of myocardial IGF-1 effects, as previously reported in other studies [ 33 , 34 ]. Immunohistochemical detection of IGF-1 expression was evaluated using a commercial kit of a polyclonal rabbit antibody (IGF-1 antibody, ab9572, Abcam, Cambridge, UK).…”

Section: Methodsmentioning

confidence: 99%

Insulin-like growth factor 1 myocardial expression decreases in chronic alcohol consumption

et al. 2013

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BackgroundAlcoholic cardiomyopathy (CMP) is one of the major complications of chronic excessive alcohol consumption. The pathogenic mechanisms implicated are diverse, inducing functional and structural changes in the myocardium. Insulin-like Growth Factor 1 (IGF-1) plays an important role in modulating the cell cycle, and helps the differentiation and proliferation of cardiac tissue inhibiting apoptosis. Experimental studies have suggested the role of IGF-1 in alcohol-induced cardiac damage. The aim of the present study was to determine the effect of chronic alcohol consumption on IGF-1 myocardial expression and to compare this expression in cases of hypertension and other cardiac diseases.MethodsWe studied heart samples from human organ donors: 10 healthy donors, 16 with hypertension, 23 with chronic alcohol consumption and 7 with other causes of cardiac disease. IGF-1 myocardial expression was evaluated with a specific immunohistochemistry assay using a semi-quantitative method.ResultsA significant decrease in IGF-1 myocardial expression was observed comparing all the cases included with control donors. This decrease in IGF-1 myocardial expression was significantly lower in the group of donors with chronic alcohol consumption compared to controls. On group evaluation according to the presence of CMP, donors with chronic alcohol consumption without CMP presented significantly lower IGF-1 expression than controls, whereas donors with chronic alcohol consumption with CMP showed a downward trend without achieving significance.ConclusionsChronic alcohol consumption significantly reduces IGF-1 myocardial expression. This decrease induced by alcohol is partially compensated in the presence of structural myocardial damage.

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Section: Methodsmentioning

confidence: 99%

Insulin-like growth factor 1 myocardial expression decreases in chronic alcohol consumption

et al. 2013

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“…27 Understanding the molecular mechanisms that regulate these processes in chondrocytes during the development of OA might lead to strategies for preventing or arresting the progression of this disease. IGF-1 is composed of 70-amino-acid straight chain, with the basic peptide with homology to human proinsulin, 29 where it is featured that its promoting the synthesis of cartilage matrix while inhibiting the matrix degradation by downregulating matrix metalloproteinases and inflammatory cytokines. In our study, initially, we established that IGF-1 was highly expressed in the chondrocytes of OA Wistar rats.…”

Section: Discussionmentioning

confidence: 99%

microRNA‐206 is required for osteoarthritis development through its effect on apoptosis and autophagy of articular chondrocytes via modulating the phosphoinositide 3‐kinase/protein kinase B‐mTOR pathway by targeting insulin‐like growth factor‐1

Zhao

et al. 2018

J of Cellular Biochemistry

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microRNA (miR) has been shown to be involved in the treatment of diseases such as osteoarthritis (OA). This study aims to investigate the role of miR‐206 in regulating insulin‐like growth factor‐1 (IGF‐1) in chondrocyte autophagy and apoptosis in an OA rat model via the phosphoinositide 3‐kinase (P13K)/protein kinase B (AKT)‐mechanistic target of rapamycin (mTOR) signaling pathway. Wistar rats were used to establish the OA rat model, followed by the observation of histopathological changes, Mankin score, and the detection of IGF‐1‐positive expression and tissue apoptosis. The underlying regulatory mechanisms of miR‐206 were analyzed in concert with treatment by an miR‐206 mimic, an miR‐206 inhibitor, or small interfering RNA against IGF‐1 in chondrocytes isolated from OA rats. Then, the expression of miR‐206, IGF‐1, and related factors in the signaling pathway, cell cycle, and apoptosis, as well as inflammatory factors, were determined. Subsequently, chondrocyte proliferation, cell cycle distribution, apoptosis, autophagy, and autolysosome were measured. OA articular cartilage tissue exhibited a higher Mankin score, promoted cell apoptotic rate, increased expression of IGF‐1, Beclin1, light chain 3 (LC3), Unc‐51‐like autophagy activating kinase 1 (ULK1), autophagy‐related 5 (Atg5), caspase‐3, and Bax, yet exhibited decreased expression of miR‐206, P13K, AKT, mTOR, and Bcl‐2. Besides, miR‐206 downregulated the expression of IGF‐1 and activated the P13K/AKT signaling pathway. Moreover, miR‐206 overexpression and IGF‐1 silencing inhibited the interleukins levels (IL‐6, IL‐17, and IL‐18), cell apoptotic rate, the formation of autolysosome, and cell autophagy while promoting the expression of IL‐1β and cell proliferation. The findings from our study provide a basis for the efficient treatment of OA by investigating the inhibitory effects of miR‐206 on autophagy and apoptosis of articular cartilage in OA via activating the IGF‐1‐mediated PI3K/AKT‐mTOR signaling pathway.

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“…The present results validated the effect of IGF-1 on EMT in HCC cells. Recently, a study showed negative correlations between IGF-1 and PDCD5 at the mRNA and protein levels ( 29 ). The study inferred that IGF-1 may downregulate the expression of PDCD5.…”

Section: Discussionmentioning

confidence: 99%

PDCD5 transfection increases cisplatin sensitivity and decreases invasion in hepatic cancer cells

Fan

Yao

et al. 2014

Oncology Letters

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Low expression levels of the programmed cell death 5 (PDCD5) gene have been reported in numerous human cancers, however, PDCD5 expression has not been investigated in hepatic cancer. The present study aims to investigate the biological behavior of PDCD5 overexpression in hepatocellular carcinoma (HCC) cells. The PDCD5 gene was stably transfected into the HepG2 HCC cell line (HepG2-PDCD5), and the expression levels of PDCD5 were examined by quantitative polymerase chain reaction and western blotting. An MTT assay was used to assess the cellular proliferating ability, and propidium iodide (PI) staining was used to evaluate the cell cycle by flow cytometry. The cells were incubated with 2 ng/ml transforming growth factor (TGF)-β for 7 days in order to induce invasion and epithelial-mesenchymal transition (EMT). Apoptosis was measured by Annexin V-fluorescein isothiocyanate and PI double labeling. A Boyden chamber invasion assay was carried out to detect tumor invasion. Western blotting was performed to detect the protein expression levels of PDCD5, insulin-like growth factor (IGF)-1 and the EMT marker, Snail. The results showed that the HepG2-PDCD5 cells exhibited slower proliferation rates and high G2/M cell numbers compared with those of the HepG2 and HepG2-Neo controls (P<0.05). The PDCD5 transfected cells showed higher sensitivity to cisplatin treatment than the HepG2-Neo cells, with a higher p53 protein expression level. PDCD5 overexpression can attenuate tumor invasion, EMT and the level of IGF-1 protein induced by TGF-β treatment. In conclusion, stable transfection of the PDCD5 gene can inhibit growth and induce cell cycle arrest in HepG2 cells, and its also notably improves the apoptosis-inducing effects of cisplatin, and reverses invasion and EMT induced by TGF-β. The use of PDCD5 is a novel strategy for improving the chemotherapeutic effects on HCC.

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Down-regulation of programmed cell death 5 by insulin-like growth factor 1 in osteoarthritis chondrocytes

Cited by 15 publications

References 33 publications

Insulin-like growth factor 1 myocardial expression decreases in chronic alcohol consumption

Insulin-like growth factor 1 myocardial expression decreases in chronic alcohol consumption

microRNA‐206 is required for osteoarthritis development through its effect on apoptosis and autophagy of articular chondrocytes via modulating the phosphoinositide 3‐kinase/protein kinase B‐mTOR pathway by targeting insulin‐like growth factor‐1

PDCD5 transfection increases cisplatin sensitivity and decreases invasion in hepatic cancer cells

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