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The heart in hypertension
Published in H. Gavras, The Year in Hypertension 2004, 2004
EDWARD D FROHLICH, HECTOR O VENTURA
BACKGROUND. Peptide hormones and growth factors are known to act by binding to cell surface receptors and subsequently activate intracellular mediators of signal transduction. Over the last three decades evidence has accumulated to indicate that at least some peptide hormones and growth factors also bind and act in the cellular interior, either after internalization by target cells or retention in their cells of synthesis. Several years ago the authors' laboratory proposed the term intracrine for such intracellularly acting peptide hormones irrespective of whether their binding/action followed internalization or occurred in the cell that sythesized them. In fact, many intracrines act in both fashions (Table 2.1).
Bioidentical hormones
Published in Climacteric, 2021
F. Z. Stanczyk, H. Matharu, S. A. Winer
In another study, indirect immunofluorescence and quantitative real-time polymerase chain reaction (qRT-PCR) were performed for labial salivary glands of healthy controls and patients with Sjögren’s syndrome to determine whether there is an intracrine pathway in healthy salivary glands that may be deranged in Sjögren’s syndrome21. The intracrine system involves the metabolism of DHEA sulfate to other androgens and to estrogens. In the control acini, immunoreactivity was localized for the following enzymes: sulfatase and sulfotransferase (in basolateral cell parts), 3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase (in basal cells parts), 5α-reductase (in acinar cell nuclei), and aromatase (in the apical cell membrane). All enzymes were more widespread in the ducts. qRT-PCR of the labial salivary glands revealed corresponding mRNAs for all the enzymes.
The use of isotretinoin for acne – an update on optimal dosing, surveillance, and adverse effects
Published in Expert Review of Clinical Pharmacology, 2020
Edileia Bagatin, Caroline Sousa Costa
The inflammation triggered by various pathways is the key and initial factor in acne pathogenesis, being present before clinical lesions [5]. Negative regulation of TLR 2 expression and reduced inflammation after topical and/or systemic treatment [32,57] has been demonstrated. The C. acnes is involved in immune response as it stimulates the antimicrobial peptides release from sebocytes and keratinocytes, as well as Th17 response [3]. It also activates the IGF1 R, increasing lipogenesis and keratinocytes proliferation [58]. The intracrine androgen production does not interfere in the serum levels and may explain the presence of acne in preadolescence and after menopause [59]. A genomic investigation by using activated SZ95 sebocytes demonstrated TLR 2 and 4 genes expression before the genes involved in lipogenesis, confirming the early occurrence of inflammatory response [60]. Increased levels of many cytokines have already been identified in skin and serum of acne patients, such as: IL-8, IL-1β, IL-17, IFNγ, IL-19 (member of IL-10 family and part of IL-17/IL-23 immune axis), and Th-17 response [3,6]. The sebum, as part of lipid content in skin surface, is important for the cutaneous barrier integrity, besides thermoregulatory, antimicrobial, and antioxidant actions [8].
Type 2 diabetes mellitus and cardiovascular risk; what the pharmacotherapy can change through the epigenetics
Published in Postgraduate Medicine, 2020
Pavlina A. Andreeva–Gateva, Ivelina D. Mihaleva, Ivanka I. Dimova
External factors from the past history of the gene activity determine the gene properties, a process termed as ‘transcriptional hysteresis’ [9]. The persistent cumulative effects on gene expression facilitate or alter responses to subsequent challenges. Self-sustaining loops refer to the auto-regulation of gene activity via their protein products [10]. Many intracrine factors, like hormones, growth factors, cytokines, enzymes, and DNA-binding proteins, can upregulate their own synthesis or the synthesis of components of their signaling systems, referred to as ‘intracrine memory’ [11]. A positive feedback loop can generate bistability, i.e. the presence of two alternative stable-activity states under identical conditions. The bistability state in the transcriptional regulation is happening if ultrasensitive molecular reactions are developed. Gene promoters bearing multiple binding sites can simultaneously react with several transcriptional factors. On the other hand, most of the transcriptional factors form dimers. Both conditions highly increase the sensitivity of the transcriptional regulation [12]. The TCF7L2 genetic locus, with the strongest known type 2 diabetes association, contains numerous enhancers that are active across a variety of cells [13].