Periostin regulates collagen fibrillogenesis and the biomechanical properties of connective tissues

Norris, Russell A.; Damon, Brook; Mironov, Vladimir; Kasyanov, Vladimir; Ramamurthi, Anand; Rodríguez, Ricardo Moreno; Trusk, Thomas C.; Potts, Jay D.; Goodwin, Richard L.; Davis, Jeff; Hoffman, Stanley; Wen, Xuejun; Sugi, Yukiko; Kern, Christine B.; Mjaatvedt, Corey H.; Turner, DP; Oka, Tôru; Conway, Simon J.; Molkentin, Jeffery D.; Forgács, Gabor; Markwald, Roger R.

doi:10.1002/jcb.21224

Cited by 542 publications

(633 citation statements)

References 70 publications

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“…Originally identified as a TGFβ-1-inducible protein specific to mouse osteoblasts [14], periostin is now recognized as a ECM component of many collagen-rich connective tissues that are subjected to mechanical stress-tension [47]. Reports of POSTN mRNA upregulation [11][12][13] and our data shown here demonstrating abundant periostin in a contractile fibrosis like DD, therefore, are not altogether unexpected.…”

Section: Discussionsupporting

confidence: 66%

“…As previously discussed, it is possible that longer-term exposure to periostin may be required to detect any significant effects on DD cell apoptosis in vitro. As periostin up-regulation is associated with connective tissues with altered mechanical stress-tension [47], it will be interesting to determine whether the combination of mechanical tension and periostin in a collagenous environment will affect DD cell avoidance of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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Periostin differentially induces proliferation, contraction and apoptosis of primary Dupuytren's disease and adjacent palmar fascia cells

Vi¹,

Feng²,

Zhu³

et al. 2009

Experimental Cell Research

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Dupuytren's disease, (DD), is a fibroproliferative condition of the palmar fascia in the hand, typically resulting in permanent contracture of one or more fingers. This fibromatosis is similar to scarring and other fibroses in displaying excess collagen secretion and contractile myofibroblast differentiation. In this report we expand on previous data demonstrating that POSTN mRNA, which encodes the extra-cellular matrix protein periostin, is up-regulated in Dupuytren's disease cord tissue relative to phenotypically normal palmar fascia. We demonstrate that the protein product of POSTN, periostin, is abundant in Dupuytren's disease cord tissue while little or no periostin immunoreactivity is evident in patient-matched control tissues. The relevance of periostin up-regulation in DD was assessed in primary cultures of cells derived from diseased and phenotypically unaffected palmar fascia from the same patients. These cells were grown in type-1 collagen-enriched culture conditions with or without periostin addition to more closely replicate the in vivo environment. Periostinwas found to differentially regulate the apoptosis, proliferation, α smooth muscle actin expression and stressed Fibroblast Populated Collagen Lattice contraction of these cell types. We hypothesize that periostin, secreted by disease cord myofibroblasts into the extra-cellular matrix, promotes the transition of resident fibroblasts in the palmar fascia toward a myofibroblast phenotype, thereby promoting disease progression.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Periostin differentially induces proliferation, contraction and apoptosis of primary Dupuytren's disease and adjacent palmar fascia cells

Vi¹,

Feng²,

Zhu³

et al. 2009

Experimental Cell Research

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“…29,30 The ability of periostin to interact and stabilize fibrillar collagens and other extracellular matrix molecules is probably a key event by which periostin controls extracellular matrix deposition and development of fibrosis. [3][4][5] We found de novo expressed periostin to colocalize and interact with integrin-b3 in glomeruli and vascular SMCs of NTS mice. Overexpression of periostin in aortic SMCs induced migration together with increased integrin-b3 expression and FAK phosphorylation.…”

Section: Discussionmentioning

confidence: 73%

“…1,2 Periostin interacts with extracellular matrix components, including collagen I, tenascin-C, and fibronectin, promoting collagen fibrillogenesis and increased strength performance of the extracellular matrix. [3][4][5] Interaction of periostin with cell-surface integrins avb3 and avb5 has been associated with increased adhesion and migration of cancer cells and vascular smooth muscle cells (SMCs). 6,7 Periostin is highly induced in vitro by TGF-b1, 1,5,8 and it was also found to be upregulated by angiotensin II in cardiac fibroblasts.…”

mentioning

confidence: 99%

NFκB-Induced Periostin Activates Integrin-β3 Signaling to Promote Renal Injury in GN

Prakoura

Kavvadas

Kormann

et al. 2016

JASN

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De novo expression in the kidney of periostin, a protein involved in odontogenesis and osteogenesis, has been suggested as a biomarker of renal disease. In this study, we investigated the mechanism(s) of induction and the role of periostin in renal disease. Using a combination of bioinformatics, reporter assay, and chromatin immunoprecipitation analyses, we found that NFkB and other proinflammatory transcription factors induce periostin expression in vitro and that binding of these factors on the periostin promoter is enriched in glomeruli during experimental GN. Mice lacking expression of periostin displayed preserved renal function and structure during GN. Furthermore, delayed administration of periostin antisense oligonucleotides in wild-type animals with GN reversed already established proteinuria, diminished tissue inflammation, and improved renal structure. Lack of periostin expression also blunted the de novo renal expression of integrin-b3 and phosphorylation of focal adhesion kinase and AKT, known mediators of integrin-b3 signaling that affect cell motility and survival, observed during GN in wild-type animals. In vitro, recombinant periostin increased the expression of integrin-b3 and the concomitant phosphorylation of focal adhesion kinase and AKT in podocytes. Notably, periostin and integrin-b3 were highly colocalized in biopsy specimens from patients with inflammatory GN. These results demonstrate that interplay between periostin and renal inflammation orchestrates inflammatory and fibrotic responses, driving podocyte damage through downstream activation of integrin-b3 signaling. Targeting periostin may be a novel therapeutic strategy for treating CKD.

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“…It is secreted into the matrix space and can activate integrins (Itg), specifically heterodimers of Itgαv with Itgβ1, Itgβ3, or Itgβ5, which in turn regulate processes such as proliferation and differentiation (Idolazzi et al, 2017). Additionally, periostin interacts with structural collagens, thereby influencing mechanical properties of the ECM (Gillan et al, 2002; Kudo, 2011; Norris et al, 2007). Its expression is controlled by mechanical stimuli and growth factors, such as transforming growth factor beta, bone morphogenetic protein 2, among other signaling molecules (Aukkarasongsup, Haruyama, Matsumoto, Shiga, & Moriyama, 2013; Ji et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Loss of periostin occurs in aging adipose tissue of mice and its genetic ablation impairs adipose tissue lipid metabolism

et al. 2018

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Remodeling of the extracellular matrix is a key component of the metabolic adaptations of adipose tissue in response to dietary and physiological challenges. Disruption of its integrity is a well‐known aspect of adipose tissue dysfunction, for instance, during aging and obesity. Adipocyte regeneration from a tissue‐resident pool of mesenchymal stem cells is part of normal tissue homeostasis. Among the pathophysiological consequences of adipogenic stem cell aging, characteristic changes in the secretory phenotype, which includes matrix‐modifying proteins, have been described. Here, we show that the expression of the matricellular protein periostin, a component of the extracellular matrix produced and secreted by adipose tissue‐resident interstitial cells, is markedly decreased in aged brown and white adipose tissue depots. Using a mouse model, we demonstrate that the adaptation of adipose tissue to adrenergic stimulation and high‐fat diet feeding is impaired in animals with systemic ablation of the gene encoding for periostin. Our data suggest that loss of periostin attenuates lipid metabolism in adipose tissue, thus recapitulating one aspect of age‐related metabolic dysfunction. In human white adipose tissue, periostin expression showed an unexpected positive correlation with age of study participants. This correlation, however, was no longer evident after adjusting for BMI or plasma lipid and liver function biomarkers. These findings taken together suggest that age‐related alterations of the adipose tissue extracellular matrix may contribute to the development of metabolic disease by negatively affecting nutrient homeostasis.

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Periostin regulates collagen fibrillogenesis and the biomechanical properties of connective tissues

Cited by 542 publications

References 70 publications

Periostin differentially induces proliferation, contraction and apoptosis of primary Dupuytren's disease and adjacent palmar fascia cells

Periostin differentially induces proliferation, contraction and apoptosis of primary Dupuytren's disease and adjacent palmar fascia cells

NFκB-Induced Periostin Activates Integrin-β3 Signaling to Promote Renal Injury in GN

Loss of periostin occurs in aging adipose tissue of mice and its genetic ablation impairs adipose tissue lipid metabolism

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