Despite the well-documented action of growth hormone-releasing hormone (GHRH) on the stimulation of production and release of growth hormone (GH), the effects of GHRH in peripheral tissues are incompletely explored. In this study, we show that GHRH plays a role in wound healing and tissue repair by acting primarily on woundassociated fibroblasts. Mouse embryonic fibroblasts (MEFs) in culture and wound-associated fibroblasts in mice expressed a splice variant of the receptors for GHRH (SV1). Exposure of MEFs to 100 nM and 500 nM GHRH or the GHRH agonist JI-38 stimulated the expression of α-smooth muscle actin (αSMA) based on immunoblot analyses as well as the expression of an αSMA-β-galactosidase reporter transgene in primary cultures of fibroblasts isolated from transgenic mice. Consistent with this induction of αSMA expression, results of transwellbased migration assays and in vitro wound healing (scratch) assays showed that both GHRH and GHRH agonist JI-38 stimulated the migration of MEFs in vitro. In vivo, local application of GHRH or JI-38 accelerated healing in skin wounds of mice. Histological evaluation of skin biopsies showed that wounds treated with GHRH and JI-38 were both characterized by increased abundance of fibroblasts during the early stages of wound healing and accelerated reformation of the covering epithelium at later stages. These results identify another function of GHRH in promoting skin tissue wound healing and repair. Our findings suggest that GHRH may have clinical utility for augmenting healing of skin wounds resulting from trauma, surgery, or disease.smooth muscle | actin | fibroblast proliferation | growth hormone G rowth hormone-releasing hormone (GHRH) is produced by the hypothalamus and acts on the pituitary, stimulating the production and release of growth hormone (GH) (1). Much evidence suggests that besides its hypophyseal action, GHRH plays a role in extrapituitary tissues and importantly in cancers stimulating tumor growth by paracrine and/or autocrine mechanisms (2, 3). Conversely, antagonistic analogs of GHRH potently inhibit the growth of various experimental human cancers in vitro and in vivo, suggesting that GHRH antagonists could serve as another specific class of anticancer agents (4).In addition to the hypothalamus, expression of GHRH has been reported in several nonhypothalamic tissues including placenta, ovaries, testes, lymphocytes, and others (5-14), but the physiological significance of this ectopic production of GHRH remains poorly elucidated. However, it has been suggested that locally produced GHRH promotes follicular maturation by paracrine modulation of the stimulatory action of follicle stimulating hormone on granulosa cell function (12), whereas in Leydig cells, GHRH contributes to spermatogenesis (9). Recent evidence also demonstrates that this neuropeptide can induce cardiac repair after myocardial infarction, by mechanisms involving a direct action on the cardiomyocytes (15, 16). Lately, it was also reported that GHRH agonists stimulate the proliferation...
Our results support the opinion that the association between psoriasis and MF does exist. It is most possibly related to the chronic lymphocyte stimulation that occurs during psoriasis that eventually leads to a dominant clone and the evolution to CTCL. Our study suggests that apart from cases of early MF, which are being indeed misdiagnosed as psoriasis, there is another group of patients, where psoriasis truly coexists with - or even progresses to - MF.
Cutaneous apocrine gland carcinoma, a subtype of sweat gland carcinoma, is a very rare malignancy, and only few cases have been reported in the literature. Many of these carcinomas are indolent and slowly developing, but some are rapidly progressive. The treatment of choice is wide local excision with clear margins, with or without lymph node dissection. We report a case of a 67-year-old man who came to our hospital with an ulcerated nodule in the right axilla measuring 1 × 0.8 cm. Histological evaluation showed features of an apocrine gland carcinoma arising in an area of high apocrine gland density.
In the routine care of Greece, infliximab reduced disease activity and improved the quality of life of moderate-to-severe psoriasis patients through 1 year of treatment, independent of their BMI and WC.
The above data confirm previous reports that treatment with infliximab is an efficacious and safe option for patients with moderate to severe plaque psoriasis (and/or arthritis). Long-term follow-up, continued pharmacovigilance, and controlled comparative studies will be required to fully evaluate its use in the treatment of psoriasis.
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