Transforming growth factor beta 1 stimulates type V collagen expression in bovine vascular smooth muscle cells

Lawrence, Romy; Hartmann, Daniel; Sonenshein, Gail E.

doi:10.1016/s0021-9258(17)36924-7

Cited by 69 publications

(5 citation statements)

References 55 publications

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“…Furthermore, RGTAs potentiated or formed complexes with heparin binding growth factors such as FGF-2 or TGF-β1 (21)(22)(23). Among several factors that may influence SMC behavior during the course of atherosclerosis, FGF-2 and TGF-β1 may play a pivotal role in altering the production of collagen by these cells (7,14,15,37). These data prompted us to look for mechanisms by which RGTAs may interact with FGF-2 and TGF-β1 to modulate the types of collagen produced by SMCs.…”

Section: Discussionmentioning

confidence: 99%

“…In particular, FGF-2 and TGF-β1 influence SMC behavior (12, 13) and are involved in the differential regulation of the collagen phenotype. Interestingly, FGF-2 selectively decreased collagen III production by SMCs ( 14), whereas TGF-β1 preferentially stimulated collagen V synthesis (15,16). These growth factors bind to heparan sulfate proteoglycans, which in turn may protect and potentiate them (17)(18)(19)(20).…”

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confidence: 99%

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Structurally different RGTAs modulate collagen‐type expression by cultured aortic smooth muscle cells via different pathways involving fibroblast growth factor‐2 or transforming growth factor‐β1

et al. 2004

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We have engineered polymers called ReGeneraTing Agents (RGTAs), which mimic the protecting and potentiating properties of heparan sulfates toward heparin-binding growth factors (HBGF). RGTAs have been shown to optimize cell growth and regulate collagen production in vitro. Here, we studied relationships between RGTA structure and collagen-type expression in aortic smooth muscle cells by using two RGTAs, the carboxylmethylsulfate dextran RG-1503 and the carboxylmethylsulfate dextran with added benzylamide RG-1192. RG-1192 specifically induced a fivefold decrease in collagen III synthesis. This effect was abolished by FGF-2 neutralizing antibody. RG-1192 and FGF-2 acted synergistically to decrease collagen III. RG-1192 was more effective than heparin in this process. RG-1192 increased the pericellular localization of FGF-2 and protected FGF-2 from proteolysis. Surface plasmon resonance analysis indicated a Kd of 15.7 nM for the RG-1192/FGF-2 interaction (10.6 nM for the heparin/FGF-2 interaction). The structurally different RG-1503 (without benzylamide) did not interact with FGF-2 and worked synergistically with TGF-beta1 to specifically induce a twofold increase in collagen V. RGTAs with different structures exert different modulating effects on the collagen phenotype. Selection of appropriate RGTAs, which had been shown to enhance in vivo tissue repair, may provide a mean of correcting collagen abnormalities in vascular disorders and more generally in fibrotic diseases.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Structurally different RGTAs modulate collagen‐type expression by cultured aortic smooth muscle cells via different pathways involving fibroblast growth factor‐2 or transforming growth factor‐β1

et al. 2004

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“…23227). For each Western blot, equal quantities of protein from each sample (12)(13)(14)(15)(16)(17)(18)(19)(20) ). All primary antibodies were produced in rabbits except for anti-GAPDH (produced in goats).…”

Section: Western Blot Analysismentioning

confidence: 99%

“…1–6 However, the mechanisms through which reduced TGF-β signaling cause aneurysms are poorly understood. Because TGF-β signaling in cultured smooth muscle cells (SMCs) increases expression of contractile proteins, 7–12 loss of SMC TGF-β signaling is expected to decrease levels of SMC contractile proteins and impair vascular contractility. Decreased functionality of the SMC contractile unit and associated impairment of vascular contractility are widely considered to be critical precursors to aortic aneurysm formation.…”

mentioning

confidence: 99%

Loss of Transforming Growth Factor Beta Signaling in Aortic Smooth Muscle Cells Causes Endothelial Dysfunction and Aortic Hypercontractility

Zhu

Angelov

Yildirim

et al. 2021

ATVB

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Objective: Humans and mice with loss-of-function variants of genes in the TGF-β (transforming growth factor beta) signaling pathway develop aortic aneurysms. These aneurysms could be caused by decreased aortic smooth muscle cell (SMC) contractile-protein levels and impaired aortic SMC contractile-unit function. Accordingly, we investigated whether loss of SMC TGF-β signaling in mice alters aortic contractile-protein levels and aortic contractility. Approach and Results: We used immunoblotting, wire myography, histological analyses, and measurements of aortic nitric oxide and superoxide levels to assess aortic contractile-protein levels and vasomotor function in mice with SMC-specific deletion of the type 2 TGF-β receptor (TBR2 SMΔ mice). Aortic contractile-protein levels were not altered in TBR2 SMΔ mice. Surprisingly, TBR2 SMΔ mice had increased aortic contractility and severe endothelial dysfunction. Endothelial dysfunction was manifested as decreased relaxation to acetylcholine (Emax 37% versus 97%; P <0.0001), decreased aortic nitric oxide (50%; P =0.005), decreased endothelial nitric oxide synthase activation (31%; P =0.002), and lower aortic levels of phosphorylated vasodilator-stimulated phosphoprotein (an indicator of nitric oxide bioavailability: 65%; P <0.0001). Aortic hypercontractility was reduced by mechanical denudation of endothelium and was eliminated by pretreatment of TBR2 SMΔ and control aortas with a nitric oxide synthase inhibitor, revealing a significant positive interaction between aortic hypercontractility and absence of endothelium-derived nitric oxide ( P <0.05 for both denudation and nitric oxide inhibition). Conclusions: Aortic aneurysms that develop in TBR2 SMΔ mice are not caused by decreased SMC contractility. Loss of physiological SMC TGF-β signaling causes endothelial dysfunction leading to aortic hypercontractility. Endothelial dysfunction may contribute to vascular pathologies associated with abnormal TGF-β signaling.

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“…The antiinflammatory cytokine, TGF-~, exerts effects on smooth muscle cells that are opposite to those of the proinflammatory ones. Thus, TGF-~ stimulates collagen [125,126] and a-actin production [127,128] and induces fibrotic hyperplasia when transfected into the arterial wall [129]. Consequently, antibodies to TGF-~ inhibit neointimal hyperplasia after mechanical injury [130,131].…”

Section: Cells and Cellular Interactionsmentioning

confidence: 99%

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Kalafatis¹,

Veer²,

Mann³

et al. 2000

Encyclopedic Reference of Vascular Biology &Amp; Pathology

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I Blood CoagulationDefinition Process that leads to clot formation. The blood coagulation system is constituted of a series of biochemical reactions that lead to the formation of fibrin. See: -.coagulation factors; _.Fibrinolytic, hemostatic and matrix metalloproteinases, role of; -.Thrombosis I BSS Definition Bernard-Soulier syndrom See: _.Bleeding disorders I CadherinsCalcium-dependent intercellular adhesion molecules. Three main types have been described, Epithelial

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Transforming growth factor beta 1 stimulates type V collagen expression in bovine vascular smooth muscle cells

Cited by 69 publications

References 55 publications

Structurally different RGTAs modulate collagen‐type expression by cultured aortic smooth muscle cells via different pathways involving fibroblast growth factor‐2 or transforming growth factor‐β1

Structurally different RGTAs modulate collagen‐type expression by cultured aortic smooth muscle cells via different pathways involving fibroblast growth factor‐2 or transforming growth factor‐β1

Loss of Transforming Growth Factor Beta Signaling in Aortic Smooth Muscle Cells Causes Endothelial Dysfunction and Aortic Hypercontractility

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