The extracellular matrix protein ?IG-H3 is expressed at myotendinous junctions and supports muscle cell adhesion

Ferguson, Jill; Thoma, Brian S.; Mikesh, Michelle F.; Kramer, Randall H.; Bennett, Kelly L.; Purchio, Anthony F.; Bellard, Bradford J.; LeBaron, Richard G.

doi:10.1007/s00441-003-0743-z

Cited by 41 publications

(31 citation statements)

References 76 publications

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“…15,16 This binding is integrin-dependent, involving a 7 b 1 . 13 The close association of ASM with these ECM components allows integrin-directed signaling from the ECM to ASM.…”

Section: Extracellular Matrix and Asm In Asthmamentioning

confidence: 99%

Synthetic responses in airway smooth muscle

Howarth

Knox²,

Amrani³

et al. 2004

Journal of Allergy and Clinical Immunology

147

105

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“…15,16 This binding is integrin-dependent, involving a 7 b 1 . 13 The close association of ASM with these ECM components allows integrin-directed signaling from the ECM to ASM.…”

Section: Extracellular Matrix and Asm In Asthmamentioning

confidence: 99%

Synthetic responses in airway smooth muscle

Howarth

Knox²,

Amrani³

et al. 2004

Journal of Allergy and Clinical Immunology

147

105

View full text Add to dashboard Cite

“…1). Through these domains and motif, TGFBI binds to integrins and other ECM proteins to mediate cell adhesion and migration [14][15][16][17][18][19][20]. Although it is present in a wide range of tissues, TGFBI is highly expressed in bone, cartilage, cornea, kidney, and skin [8,21].…”

mentioning

confidence: 99%

Targeted Disruption of TGFBI in Mice Reveals Its Role in Regulating Bone Mass and Bone Size through Periosteal Bone Formation

Wergedal

Zhao

et al. 2012

Calcif Tissue Int

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Transforming growth factor-beta induced (TGFBI) and periostin are two closely related proteins in structure as well as in function. A previous study found that periostin positively regulates bone size. Here, we hypothesize that TGFBI has a similar function in bone development. To test this hypothesis, we employed TGFBI-deficient mice, which were generated by targeted disruption of the TGFBI gene. We bred these mice with C57BL/6J mice to generate homozygous TGFBI-deficient (TGFBI(-/-)) mice and homozygous wild-type littermates. All mice were raised to 12 weeks of age. Bone mass parameters were determined by PIXImus and micro-CT, bone strength parameters by three-point bending, and bone formation and resorption parameters by histomorphometry. We found that targeted disruption of TGFBI led to reduced body size, bone mass, bone size, and bone strength. This indicates that, like periostin, TGFBI also positively regulates bone size and that changes in bone size affect bone strength. Furthermore, there was also a significant decrease in periosteal, but not endosteal, bone formation rate of cortical bone in TGFBI(-/-) mice, suggesting that the observed effect of TGFBI on bone mass and bone size was largely caused by the effect of TGFBI on periosteal bone formation.

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“…Although the types of its interacting integrins have not been pinpointed (25,26), in theory, the RGD domain should be able to interact with a5b1, a8b1, aVb3, aVb5, aVb6, aVb8, and aIIb3 (27). TGF-bi is also known to bind to a1b1, a6b4, a7b1 (28)(29)(30), but domain(s) involved in such associations have not been re-ported. Thus, secreted TGF-bi acts as a bifunctional molecule enhancing ECM and cell interactions, a lack of which results in dysfunction of many cell types.…”

mentioning

confidence: 99%

TGF-βi Promotes Islet β-Cell Function and Regeneration

Han

et al. 2011

The Journal of Immunology

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TGF-βi is a secreted protein and is capable of binding to both extracellular matrix (ECM) and cells. It thus acts as a bifunctional molecule enhancing ECM and cell interactions, a lack of which results in dysfunction of many cell types. In this study, we investigated the role of TGF-βi in the function and survival of islets. Based on DNA microarray followed by quantitative PCR confirmation, TGFβi gene showed drastic increase in expression in islets after culture. We demonstrated that recombinant TGF-βi could preserve the integrity and enhance the function of cultured islets. Such a beneficial effect was mediated via signaling through FAK. Exogenous TGF-βi was capable of sustaining high-level FAK phosphorylation in isolated islets, and FAK knockdown by small interfering RNA in islets resulted in compromised islet function. TGF-βi transgenic (Tg) islets showed better integrity and insulin release after in vitro culture. In vivo, β-cell proliferation was detectable in Tg but not wild-type pancreata. At age above 12 mo, Tg pancreata contained giant islets. Tg mice displayed better glucose tolerance than that of the controls. Tg islets were more potent in lowering blood glucose when transplanted into syngeneic mice with streptozotocin-induced diabetes, and these transplanted islets also underwent regeneration. Our results indicate that TGF-βi is a vital trophic factor promoting islet survival, function, and regeneration. At least some of its beneficial effect was mediated by signaling through FAK.

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The extracellular matrix protein ?IG-H3 is expressed at myotendinous junctions and supports muscle cell adhesion

Cited by 41 publications

References 76 publications

Synthetic responses in airway smooth muscle

Synthetic responses in airway smooth muscle

Targeted Disruption of TGFBI in Mice Reveals Its Role in Regulating Bone Mass and Bone Size through Periosteal Bone Formation

TGF-βi Promotes Islet β-Cell Function and Regeneration

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