Periodic mechanical stress activates MEK1/2-ERK1/2 mitogenic signals in rat chondrocytes through Src and PLCγ1

Huang, Yu‐Min; Liang, Wen-Wei; Liu, Feng; Wang, Qing; Cui, Weiding; Liu, Zhengyu; Yin, Guoyong; Fan, Weimin

doi:10.1590/s0100-879x2011007500150

Cited by 16 publications

(16 citation statements)

References 34 publications

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“…The findings of Ren et al (15) indicated that periodic mechanical stress activated the Src-PLCγ1-mitogen-activated protein kinase kinase (MEK)1/2-ERK1/2 signaling pathway to induce chondrocyte proliferation and matrix synthesis. In addition, the study of Ren et al (25) demonstrated that the Src-PLCγ1-MEK1/2 signaling pathway involved chondrocyte area expansion and migration using periodic mechanical stress. GIT1, present in mammals and birds, is a multidomain scaffold protein that participates in the internalization and membrane transportation of G protein-coupled recep-tors (7)(8)(9)(10)(11).…”

Section: Discussionmentioning

confidence: 99%

Effects of platelet-derived growth factor on chondrocyte proliferation, migration and apoptosis via regulation of GIT1 expression

Zhao

Zhang

Liu

et al. 2016

Molecular Medicine Reports

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The formation of fibrocartilage, cartilaginous and bony calluses is vital for bone healing following a fracture. Fibroblasts, chondrocytes and osteoblasts are critical functional cells that are involved in these three processes, respectively. Platelet‑derived growth factor (PDGF), a growth factor that is released from platelet particles and appears during the early stages at the site of fractures, is essential in bone healing via regulation of cell proliferation and differentiation. However, the effects of PDGF on the chondrocytes remain unclear. In the present study, PDGF promoted phosphorylation of Src and upregulated the expression level of G‑protein‑coupled receptor kinase interacting protein‑1 (GIT1) according to the results of the cell culture of chondrocytes in vitro and western blotting. However, the effect of PDGF on the upregulation of GIT1 expression was mostly inhibited by the Src inhibitor, PP2. After knocking down GIT1 expression using siRNA, the phosphorylation of Src continued to be induced by PDGF, although the expression of GIT1 was inhibited. Furthermore, the results indicated that PDGF promoted chondrocyte proliferation and migration, however, the effect on cell apoptosis induction was suppressed after adding the Src inhibitor, PP2. Additionally, when knocking down GIT1 using siRNA, the expression level of GIT1 decreased, which is similar to the effect of the Src inhibitor, PP2. The current study demonstrates that PDGF may initially activate the phosphorylation of Src, and subsequently induce GIT1 expression to promote chondrocyte proliferation and migration, but suppress cell apoptosis.

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Section: Discussionmentioning

confidence: 99%

Effects of platelet-derived growth factor on chondrocyte proliferation, migration and apoptosis via regulation of GIT1 expression

Zhao

Zhang

Liu

et al. 2016

Molecular Medicine Reports

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“…Integrins, including α1β1, α5β1, α10β1 and αVβ5, are mainly expressed in the articular cartilage in healthy adults (15,16). In addition, the study by Ren et al (17) provided evidence that periodic mechanical stress induces the activation of the integrin-β1-Src-PLCγ1/Rac1-mediated extracellular signal-regulated kinase 1/2 (ERK1/2) mitogenic signaling pathway, enhancing chondrocyte proliferation and matrix synthesis. Taken together, these data suggest that there is a close association between GIT1 and integrins in bone cells.…”

Section: Introductionmentioning

confidence: 99%

Integrin-β1 regulates chondrocyte proliferation and apoptosis through the upregulation of GIT1 expression

Zhang

Zhao

et al. 2015

International Journal of Molecular Medicine

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Chondrocytes play a critical role in the repair process of osteoarthritis, which is also known as degenerative arthritis. Integrins, as the key family of cell surface receptors, are responsible for the regulation of chondrocyte proliferation, differentiation, survival and apoptosis through the recruitment and activation of downstream adaptor proteins. Moreover, G-protein-coupled receptor kinase interacting protein-1 (GIT1) exerts its effects on cell proliferation and migration through interaction with various cytokines. It has been previously suggested that GIT1 acts as a vital protein downstream of the integrin-mediated pathway. In the present study, we investigated the effects of integrin-β1 on cell proliferation and apoptosis, as well as the underlying mechanisms in chondrocytes in vitro. Following transfection with a vector expressing integrin-β1, our results revealed that the overexpression of integrin-β1 enhanced GIT1 expression, whereas the knockdown of integrin-β1 by siRNA suppressed GIT1 expression. However, no significant effect was observed on integrin-β1 expression following the enforced overexpression of GIT1, which suggests that GIT1 is localized downstream of integrin-β1. In other words, integrin-β1 regulates the expression of GIT1. Furthermore, this study demonstrated that integrin-β1 and GIT1 increased the expression levels of aggrecan and type II collagen, thus promoting chondrocyte proliferation; however, they inhibited chondrocyte apoptosis. Taken together, our data demonstrate that integrin-β1 plays a vital role in chondrocyte proliferation, differentiation and apoptosis. GIT1 exerts effects similar to those of integrin-β1 and is a downstream target of integrin-β1.

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“…et al 20 explored the signal transduction pathways of chondrocyte proliferation and matrix synthesis under periodic mechanical stress endeavoring to identify the role of the MEK1/2-ERK1/2 signaling pathway in chondrocyte proliferation and matrix synthesis following cyclic physiologic mechanical compression. Their findings suggest that periodic mechanical stress promotes chondrocyte proliferation and matrix synthesis in part through the Src-PLCγ1-MEK1/2-ERK1/2 signaling pathway, which links these three important signaling molecules into a mitogenic cascade.…”

Section: General Reviewmentioning

confidence: 99%

[ARTIGO RETRATADO] Revisão dos artigos sobre ortopedia recentemente publicados na imprensa científica brasileira

Rocha-e-Silva

Gomes

2012

Acta ortop. bras.

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This paper is a review of articles published in Brazilian scientific periodicals in recent years. Its main purpose is to bring to the attention of the readership of Acta Ortopedica Brasileira original contributions to the field published in non-specialized journals. We hope that this will serve as a general scientific update for readers. The review includes works published in six ISI indexed non-orthopedic journals, following a literature search conducted in fourteen such journals.

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Periodic mechanical stress activates MEK1/2-ERK1/2 mitogenic signals in rat chondrocytes through Src and PLCγ1

Cited by 16 publications

References 34 publications

Effects of platelet-derived growth factor on chondrocyte proliferation, migration and apoptosis via regulation of GIT1 expression

Effects of platelet-derived growth factor on chondrocyte proliferation, migration and apoptosis via regulation of GIT1 expression

Integrin-β1 regulates chondrocyte proliferation and apoptosis through the upregulation of GIT1 expression

[ARTIGO RETRATADO] Revisão dos artigos sobre ortopedia recentemente publicados na imprensa científica brasileira

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