Expression of type I collagen and tenascin C is regulated by actin polymerization through MRTF in dedifferentiated chondrocytes

Parreno, Justin; Raju, Sneha; Niaki, Mortah Nabavi; Andrejevic, Katarina; Jiang, Aiting; Delve, E.; Kandel, Rita A.

doi:10.1016/j.febslet.2014.08.012

Cited by 43 publications

(80 citation statements)

References 34 publications

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“…Furthermore, loss of CDH11 either in Cdh11 −/− mouse dermal fibroblasts or in shCDH11 human dermal fibroblasts abolished the expression of transcription factors known to affect ECM synthesis (Ueyama et al, 2003;Medjkane et al, 2009;Small et al, 2010;Leitner et al, 2011;Velasquez et al, 2013;Johnson et al, 2014;Parreno et al, 2014), such as MYOCD, MRTF-A, SRF and to a lesser extent MRTF-B. In agreement, knocking down either MYOCD or MRTF-A and -B decreased CDH11-mediated expression of collagen and elastin, but the effects of MRTF-A and -B were significantly stronger.…”

Section: Discussionmentioning

confidence: 57%

Cadherin-11 is a novel regulator of extracellular matrix synthesis and tissue mechanics

Row

Liu

Alimperti

et al. 2016

Journal of Cell Science

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We discovered that Cadherin-11 (CDH11) regulates collagen and elastin synthesis, both affecting the mechanical properties and contractile function of animal tissues. Using a Cdh11-null mouse model, we observed a significant reduction in the mechanical properties [Youngs' modulus and ultimate tensile strength (UTS)] of Cdh11 −/− as compared to wild-type (WT) mouse tissues, such as the aorta, bladder and skin. The deterioration of mechanical properties (Youngs' modulus and UTS) was accompanied by reduced collagen and elastin content in Cdh11 −/− mouse tissues as well as in cells in culture. Similarly, knocking down CDH11 abolished collagen and elastin synthesis in human cells, and consequently reduced their ability to generate force. Conversely, engagement of CDH11 through homophilic interactions, led to swift activation of the TGF-β and ROCK pathways as evidenced by phosphorylation of downstream effectors. Subsequently, activation of the key transcription factors, MRTF-A (also known as MKL1) and MYOCD led to significant upregulation of collagen and elastin genes. Taken together, our results demonstrate a novel role of adherens junctions in regulating extracellular matrix (ECM) synthesis with implications for many important biological processes, including maintenance of tissue integrity, wound healing and tissue regeneration.

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Section: Discussionmentioning

confidence: 57%

Cadherin-11 is a novel regulator of extracellular matrix synthesis and tissue mechanics

Row

Liu

Alimperti

et al. 2016

Journal of Cell Science

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“…2a; right panel and 2B). To further confirm these changes in the actin cytoskeleton, we quantified levels of F- and G-actin using selective solubilisation of G-actin in Triton-X-100, as previously described 37 . This demonstrated that forskolin stimulation of VSMC resulted in a significant reduction in F-actin and a significant increase in G-actin (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…F- and G-actin were separated by triton solubility essentially as previously 37 described with slight modifications. Following treatment, G-actin was extracted in G-actin extraction buffer (PBS, 10% glycerol, 0.1% triton X-100, 1 mM ATP and complete protease inhibitor) and incubated for 5 min at room temperature with slight agitation.…”

Section: Methodsmentioning

confidence: 99%

Divergent Regulation of Actin Dynamics and Megakaryoblastic Leukemia-1 and -2 (Mkl1/2) by cAMP in Endothelial and Smooth Muscle Cells

Smith

Hudson

Kimura

et al. 2017

Sci Rep

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Proliferation and migration of vascular smooth muscle cells (VSMCs) or endothelial cell (ECs) promote or inhibit, respectively, restenosis after angioplasty, vein graft intimal thickening and atherogenesis. Here we investigated the effects of cAMP-induced cytoskeletal remodelling on the serum response factor (SRF) co-factors Megakaryoblastic Leukemia-1 and -2 (MKL1 and MKL2) and their role in controlling VSMC and EC proliferation and migration. Elevation of cAMP using forskolin, dibutyryl-cAMP (db-cAMP), BAY60-6583 or Cicaprost induced rapid cytoskeleton remodelling and inhibited proliferation and migration in VSMCs but not EC. Furthermore, elevated cAMP inhibited mitogen-induced nuclear-translocation of MKL1 and MKL2 in VSMCs but not ECs. Forskolin also significantly inhibited serum response factor (SRF)-dependent reporter gene (SRE-LUC) activity and mRNA expression of pro-proliferative and pro-migratory MKL1/2 target genes in VSMCs but not in ECs. In ECs, MKL1 was constitutively nuclear and MKL2 cytoplasmic, irrespective of mitogens or cAMP. Pharmacological or siRNA inhibition of MKL1 significantly inhibited the proliferation and migration of VSMC and EC. Our new data identifies and important contribution of MKL1/2 to explaining the strikingly different response of VSMCs and ECs to cAMP elevation. Elucidation of these pathways promises to identify targets for specific inhibition of VSMC migration and proliferation.

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“…Hydrogels are particularly convenient since they induce cell rounding and round morphology associated with depolymerized actin is essential for correct chondrogenic expression . On the contrary, in a 2D environment such as a phase of cellular expansion on plastic, chondrocytes adopt a fibroblastic shape associated with polymerized actin and this results in chondrocyte dedifferentiation . In this study, we hypothesized that an SAP IEIK13 hydrogel would provide an appropriate 3D environment for encapsulation of chondrocytes.…”

Section: Discussionmentioning

confidence: 99%

Combination of bioactive factors and IEIK13 self‐assembling peptide hydrogel promotes cartilage matrix production by human nasal chondrocytes

Dufour

Buffier²,

Vertu-Ciolino

et al. 2019

J Biomedical Materials Res

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Nasal reconstruction remains a challenge for every reconstructive surgeon. Alloplastic implants are proposed to repair nasal cartilaginous defects but they are often associated with high rates of extrusion and infection and poor biocompatibility. In this context, a porous polymeric scaffold filled with an autologous cartilage gel would be advantageous. In this study, we evaluated the capacity of IEIK13 self‐assembling peptide (SAP) to serve as support to form such cartilage gel. Human nasal chondrocytes (HNC) were first amplified with FGF‐2 and insulin, and then redifferentiated in IEIK13 with BMP‐2, insulin, and T3 (BIT). Our results demonstrate that IEIK13 fosters HNC growth and survival. HNC phenotype was assessed by RT‐PCR analysis and neo‐synthesized extracellular matrix was characterized by western blotting and immunohistochemistry analysis. BIT‐treated cells embedded in IEIK13 displayed round morphology and expressed cartilage‐specific markers such as type II and type IX collagens and aggrecan. In addition, we did not detect significant production of type I and type X collagens and gene products of dedifferentiated and hypertrophic chondrocytes that are unwanted in hyaline cartilage. The whole of these results indicates that the SAP IEIK13 represents a suitable support for hydrogel‐based tissue engineering of nasal cartilage. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 893–903, 2019.

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Expression of type I collagen and tenascin C is regulated by actin polymerization through MRTF in dedifferentiated chondrocytes

Cited by 43 publications

References 34 publications

Cadherin-11 is a novel regulator of extracellular matrix synthesis and tissue mechanics

Cadherin-11 is a novel regulator of extracellular matrix synthesis and tissue mechanics

Divergent Regulation of Actin Dynamics and Megakaryoblastic Leukemia-1 and -2 (Mkl1/2) by cAMP in Endothelial and Smooth Muscle Cells

Combination of bioactive factors and IEIK13 self‐assembling peptide hydrogel promotes cartilage matrix production by human nasal chondrocytes

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