A Fibronectin-Independent Mechanism of Collagen Fibrillogenesis in Adult Liver Remodeling

Moriya, Kei; Bae, Eunnyung; Honda, Kazuhisa; Sakai, Keiko; Sakaguchi, Takehisa; Tsujimoto, Ikuko; Kamisoyama, Hiroshi; Keene, Douglas R.; Sasaki, Takako; Sakai, Takao

doi:10.1053/j.gastro.2011.02.005

Cited by 62 publications

(96 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Acute liver injury was induced intraperitoneously by a single-dose administration of carbon tetrachloride [CCl 4 ; 1.0 ml/kg body weight as a 50% (v/v) solution in olive oil (Fluka)] in sex-matched mice as described previously. 15 …”

Section: Mice and Induction Of Acute Liver Injury By Carbon Tetrachlomentioning

confidence: 99%

“…15,16 To quantify positive areas in response to acute liver injury, images were captured with the same gain, offset, magnitude and exposure time. Then a minimum of four different images from each mouse were randomly selected and the intensities were quantified using Image-Pro Plus software version 6.1 (Media Cybernetics, Bethesda, MA).…”

Section: Histological Analysis Immunohistochemistry and Immunofluormentioning

confidence: 99%

“…Immunoreactive bands were detected using the Odyssey Infrared Imaging System (LI-COR Bioscience) as described previously. 15 …”

Section: One-and Two-dimensional Sds-page and Western Blot Analysismentioning

confidence: 99%

See 2 more Smart Citations

Critical Role of Factor XIII in the Initial Stages of Carbon Tetrachloride–Induced Adult Liver Remodeling

Tsujimoto

Moriya

Sakai

et al. 2011

The American Journal of Pathology

Self Cite

View full text Add to dashboard Cite

The transglutaminase-mediated, covalent cross-linking of proteins is an essential step in tissue remodeling after injury. This process provides tissues with extra rigidity and resistance against proteolytic degradation. Plasma coagulation factor XIII (FXIII) is a transglutaminase that promotes cross-linking of the extracellular matrix (ECM) components fibrin and fibronectin to form a provisional matrix in response to tissue damage. However, the functional requirement for this FXIII-mediated cross-linked provisional matrix in adult tissue remodeling remains to be defined. Although it has been proposed that the formation FXIII-mediated fibrin-fibronectin provisional matrix is a critical step for ECM remodeling, we show in an FXIII subunit A-deficient murine model of acute liver injury that the lack of FXIII subunit A did not interfere with collagen reconstruction and resolution after liver injury. Furthermore, FXIIIA deficiency caused significantly increased hepatocyte apoptosis and a delay in hepatocyte regeneration after injury, which were accompanied by a significantly high induction of p53 expression. These findings suggest novel functions of FXIII that the FXIII-mediated covalently crosslinked matrix could promote survival signals for hepatocytes in adult tissue remodeling. Covalent cross-linking between proteins, including in the provisional matrix, is catalyzed by transglutaminases (TGs). This is an important process for tissue remodeling as it generates extra rigidity and a resistance against proteolytic degradation. 1 Plasma coagulation factor Xlll (FXlll), one of the TG family members, circulates as a heterotetramer composed of two catalytic A subunits (FXIII A) and two noncatalytic B subunits (FXIII B) (A 2 B 2 ), which are activated by thrombinmediated cleavage. FXlll is a Ca 2ϩ -dependent TG and catalyzes the formation of -(␥-glutamyl) lysyl crosslinks between specific protein pairs. The cross-linking of fibrin molecules by FXIII to form ␥-chain dimerization is the final step of blood coagulation. 2-4 FXIII also acts on fibronectin-fibronectin and fibrin-fibronectin cross-linking. 5,6 Thus, the action of FXIII in forming covalent crosslinkages clearly plays a vital role in establishing the mechanical stability of the clot, which is critical for homeostatic functions. 2,4 Growing evidence demonstrates that the source of FXIII is not only from plasma: Megakaryocytes/ platelets and monocytes/macrophages also contain cellular FXIII subunit A in their cytoplasm. 7,8 Acute liver injury mediated by the hepatitis virus or hepatotoxins causes massive hepatocyte apoptosis and/or fatal liver damage, and eventually liver transplantation is required. 9,10 Identification of hepatic survival factors is critical for successful therapeutic intervention in liver failure. After acute injury, the liver undergoes a wound-healing response to restore tissue architecture and maintain homeostasis. 11 It requires both a well-orchestrated proliferation of cells and the reconstruction of the extracellular matrix (ECM). A central...

show abstract

Section: Mice and Induction Of Acute Liver Injury By Carbon Tetrachlomentioning

confidence: 99%

Section: Histological Analysis Immunohistochemistry and Immunofluormentioning

confidence: 99%

See 1 more Smart Citation

Critical Role of Factor XIII in the Initial Stages of Carbon Tetrachloride–Induced Adult Liver Remodeling

Tsujimoto

Moriya

Sakai

et al. 2011

The American Journal of Pathology

Self Cite

View full text Add to dashboard Cite

show abstract

“…6,15 All mice were maintained and bred at the animal facility in accordance with institutional guidelines. Mice were regularly monitored and had free access to standard mouse chow and water.…”

Section: Micementioning

confidence: 99%

“…The networks were found to be nucleated by type V collagen, induced by elevated local transforming growth factor (TGF)-b bioavailability. 6 Therefore, we identified two mechanisms of collagen fibrillogenesis in response to liver injury: both fibronectin and TGF-besignaling mediated. Early in the fibrogenic process, inflammatory cytokines are important in initiating repair following injury.…”

mentioning

confidence: 99%

Transforming Growth Factor-β–Independent Role of Connective Tissue Growth Factor in the Development of Liver Fibrosis

Sakai

Jawaid

Sasaki

et al. 2014

The American Journal of Pathology

Self Cite

View full text Add to dashboard Cite

We previously identified transforming growth factor (TGF)-b signaling as a fibronectin-independent mechanism of type I collagen fibrillogenesis following adult liver injury. To address the contribution of TGF-b signaling during the development of liver fibrosis, we generated adult mice lacking TGF-b type II receptor (TGF-bIIR) from the liver. TGF-bIIR knockout livers indeed showed a dominant effect in reducing fibrosis, but fibrosis still remained approximately 45% compared with control and fibronectin knockout livers. Unexpectedly, this was accompanied by significant up-regulation of connective tissue growth factor mRNA levels. Organized type I collagen networks in TGF-bIIR knockout livers colocalized well with fibronectin. We provide evidence that elimination of TGF-bIIR is not sufficient to completely prevent liver fibrosis. Our results indicate a TGF-beindependent mechanism of type I collagen production and suggest connective tissue growth factor as its potent mediator. We advocate combined elimination of TGF-b signaling and connective tissue growth factor as a potential therapeutic target by which to attenuate liver fibrosis. (Am J Pathol 2014 http://dx

show abstract

Type V Collagen in Health, Disease, and Fibrosis

Mak

Png

Lee

2016

The Anatomical Record

137

View full text Add to dashboard Cite

Type V collagen (COLV) is a regulatory fibril-forming collagen. It has at least three different molecular isoforms-a1(V) 2 a2(V), a1(V) 3, and a1(V)a2(V)a3(V)-formed by combinations of three different polypeptide a chains-a1(V), a2(V), and a3(V). COL V is a relatively minor collagen of the extracellular matrix (ECM). Morphologically, COLV occurs as heterotypic fibrils with type I collagen (COLI), microfilaments, or 12-nm-thick fibrils. COLV is synthesized in various mesenchymal cells and its gene expression is modulated by TGF-b and growth factors. While resistant to digestion by interstitial collagenases, native and denatured COLV are degraded by metalloproteinases and gelatinases, thereby promoting ECM remodeling. COLV interacts with matrix collagens and structural proteins, conferring structural integrity to tissue scaffolds. It binds matrix macromolecules, modulating cellular behavior, and functions. COLV coassembles with COLI into heterotypic fibrils in the cornea and skin dermis, acting as a dominant regulator of collagen fibrillogenesis. COLV deficiency is associated with loss of corneal transparency and classic EhlersDanlos syndrome, while COLV overexpression is found in cancer, granulation tissue, inflammation, atherosclerosis, and fibrosis of lungs, skin, kidneys, adipose tissue, and liver. COLV isoform containing the a3(V) chain is involved in mediating pancreatic islet cell functions. In the liver, COLV is a minor but regular component of the ECM. Increases in COLV are associated with both early and advanced hepatic fibrosis. The neoepitopes of COLV have been shown to be a useful noninvasive serum biomarker for assessing fibrotic progression and resolution in experimental hepatic fibrosis. COLV is multifunctional in health, disease, and fibrosis. Anat Rec, 299:613-629, 2016. V C 2016 Wiley Periodicals, Inc.Key words: collagen V synthesis and degradation; collagen V deficiency and overexpression; collagen V in disease and fibrosis; collagen V neoepitopes; hepatic fibrosis biomarker

show abstract

A Fibronectin-Independent Mechanism of Collagen Fibrillogenesis in Adult Liver Remodeling

Cited by 62 publications

References 41 publications

Critical Role of Factor XIII in the Initial Stages of Carbon Tetrachloride–Induced Adult Liver Remodeling

Critical Role of Factor XIII in the Initial Stages of Carbon Tetrachloride–Induced Adult Liver Remodeling

Transforming Growth Factor-β–Independent Role of Connective Tissue Growth Factor in the Development of Liver Fibrosis

Type V Collagen in Health, Disease, and Fibrosis

Contact Info

Product

Resources

About