The role of histamine in the regulation of the viability, proliferation and transforming growth factor β1 secretion of rat wound fibroblasts

Wolak, Monika; Bojanowska, Ewa; Staszewska, Teresa; Ciosek, Joanna; Juszczak, Marlena; Drobnik, Jacek

doi:10.1016/j.pharep.2016.11.006

Cited by 13 publications

(21 citation statements)

References 35 publications

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“…Our previous study has shown that MC-derived histamine regulates TGF-β1 1 , but our current study also demonstrates a link between H1HR and TGF-β1. To support our findings, during would healing, histamine increased TGF-β1 in fibroblasts, which was blocked by pre-treatment with an H1HR inhibitor 42 . Our studies found that increased biliary TGF-β1 was induced by histamine treatment both in vitro and in vivo and since cholangiocytes express HDC and secrete histamine 22 , we suspect that histamine treatment in DKO mice may regulate biliary TGF-β1 via H1HR/PKC-α signaling since TGF-β1 activation was reduced with H1HR inhibition.…”

Section: Discussionsupporting

confidence: 85%

Biliary damage and liver fibrosis are ameliorated in a novel mouse model lacking l-histidine decarboxylase/histamine signaling

Kennedy

Meadows

Demieville

et al. 2020

Laboratory Investigation

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Primary sclerosing cholangitis (PSC) is characterized by biliary damage and fibrosis. Multidrug resistance-2 gene knockout (Mdr2 −/− ) mice and PSC patients have increased histamine (HA) levels (synthesized by l-histidine decarboxylase, HDC) and HA receptor (HR) expression. Cholestatic HDC −/− mice display ameliorated biliary damage and hepatic fibrosis. The current study evaluated the effects of knockout of HDC −/− in Mdr2 −/− mice (DKO) on biliary damage and hepatic fibrosis. WT, Mdr2 −/− mice and homozygous DKO mice were used. Selected DKO mice were treated with HA. We evaluated liver damage along with HDC expression and HA serum levels. Changes in ductular reaction were evaluated along with liver fibrosis, inflammation and bile acid signaling pathways. The expression of H1HR/PKC-α/TGF-β1 and H2HR/pERK/VEGF-C was determined. In vitro , cholangiocyte lines were treated with HA with/without H1/H2 inhibitors before measuring: H1/H2HR, TGF-β1 and VEGF-C expression. Knockout of HDC ameliorates hepatic damage, ductular reaction, fibrosis, inflammation, bile acid signaling and H1HR/PKC-α/TGF-β1 and H2HR/pERK/VEGF-C signaling. Reactivation of the HDC/HA axis increased these parameters. In vitro , stimulation with HA increased HR expression and PKC-α, TGF-β1 and VEGF-C expression, which was reduced with HR inhibitors. Our data demonstrate the key role for the HDC/HA axis in the management of PSC progression.

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Section: Discussionsupporting

confidence: 85%

Biliary damage and liver fibrosis are ameliorated in a novel mouse model lacking l-histidine decarboxylase/histamine signaling

Kennedy

Meadows

Demieville

et al. 2020

Laboratory Investigation

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“…These findings suggest that histamine targeting has pharmacological potential. In addition, histamine participates in the wound-healing process by increasing the viability of rat wound fibroblasts and promoting the production of TGF- β in an H1R-dependent manner [ 63 ].…”

Section: Regulatory and Immunomodulatory Functions Of Histaminementioning

confidence: 99%

Role of Histamine in Modulating the Immune Response and Inflammation

Branco

Yoshikawa

Pietrobon

et al. 2018

Mediators of Inflammation

251

187

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Inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, and leukotrienes, impact the immune system, usually as proinflammatory factors. Other mediators act as regulatory components to establish homeostasis after injury or prevent the inflammatory process. Histamine, a biogenic vasoactive amine, causes symptoms such as allergies and has a pleiotropic effect that is dependent on its interaction with its four histamine receptors. In this review, we discuss the dualistic effects of histamine: how histamine affects inflammation of the immune system through the activation of intracellular pathways that induce the production of inflammatory mediators and cytokines in different immune cells and how histamine exerts regulatory functions in innate and adaptive immune responses. We also evaluate the interactions between these effects.

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“…Our earlier experiments performed on cells isolated from wound models confirmed that histamine accelerates the metabolism of the cells and increases TGFβ1 secretion [12]. This effect was not seen in cultures of naïve fibroblasts derived from the intact skin of rats [12]. Some other studies have shown that histamine may modulate collagen synthesis in human dermal fibroblast cultures [13] or in skin fibroblasts derived from guinea pigs [14].…”

Section: Introductionmentioning

confidence: 83%

“…Secondly, histamine may increase collagen synthesis by exerting a direct influence on the granulation tissue cells responsible for the synthesis of the extracellular matrix. Our earlier experiments performed on cells isolated from wound models confirmed that histamine accelerates the metabolism of the cells and increases TGFβ1 secretion [12]. This effect was not seen in cultures of naïve fibroblasts derived from the intact skin of rats [12].…”

Section: Introductionmentioning

confidence: 89%

Histamine augments collagen content via H1 receptor stimulation in cultures of myofibroblasts taken from wound granulation tissue

et al. 2020

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The inflammatory reaction influences the deposition of collagen within wound granulation tissue. The aim of the present study is to determine whether histamine acting directly on myofibroblasts derived from wound granulation tissue may influence collagen deposition. It also identifies the histamine receptor involved in this process. The experiments were carried out on cells isolated from the granulation tissue of a wound model (a polypropylene net inserted subcutaneously to rats) or intact rat skin. Collagen content was measured following the addition of different concentrations of histamine and treatment with histamine receptor antagonists (ketotifen – H1 inhibitor, ranitidine – H2 inhibitor) and a histamine receptor H1 agonist (2-pyridylethylamine dihydrochloride).The cells were identified as myofibroblasts: alpha-smooth muscle actin, vimentin, and desmin positive in all experimental conditions. Histamine increased the collagen level within both cell cultures, i.e., those isolated from granulation tissue or intact skin. It did not, however, influence the expression of either the collagen type I or III genes within the cultured myofibroblasts. Histamine activity was reduced by ketotifen (the H1 receptor inhibitor) and increased by the H1 receptor agonist, as demonstrated by changes in the levels of collagen in the myofibroblast culture. Histamine increased collagen content within the cultures, acting directly on myofibroblasts via H1 receptor stimulation.

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The role of histamine in the regulation of the viability, proliferation and transforming growth factor β1 secretion of rat wound fibroblasts

Cited by 13 publications

References 35 publications

Biliary damage and liver fibrosis are ameliorated in a novel mouse model lacking l-histidine decarboxylase/histamine signaling

Biliary damage and liver fibrosis are ameliorated in a novel mouse model lacking l-histidine decarboxylase/histamine signaling

Role of Histamine in Modulating the Immune Response and Inflammation

Histamine augments collagen content via H1 receptor stimulation in cultures of myofibroblasts taken from wound granulation tissue

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