Testosterone regulates levels of cystic fibrosis transmembrane regulator, adenylate cyclase, and cAMP in the seminal vesicles of orchidectomized rats

Ramli, Norlisah; Giribabu, Nelli; Muniandy, Sekaran; Salleh, Naguib

doi:10.1016/j.theriogenology.2015.09.036

Cited by 11 publications

(5 citation statements)

References 35 publications

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“…Both oestrogen and progesterone, through functional regulation of ion transporters, further dehydrate the airway–surface liquid, a crucial ingredient for optimal mucociliary clearance, which when impaired confers a susceptibility to microbial colonisation and infection [ 62 , 102 – 106 ]. Testosterone and female sex steroid hormones also differentially regulate levels of CFTR expression in the lungs and other organs [ 107 , 108 ]. R amli et al [ 107 ] demonstrate that testosterone increases CFTR epithelial expression, an effect reversed by anti-androgen treatment with flutamide.…”

Section: Gender Differences In Cf and Non-cf Bronchiectasismentioning

confidence: 99%

“…Testosterone and female sex steroid hormones also differentially regulate levels of CFTR expression in the lungs and other organs [ 107 , 108 ]. R amli et al [ 107 ] demonstrate that testosterone increases CFTR epithelial expression, an effect reversed by anti-androgen treatment with flutamide. Similar effects with oestrogen but not progesterone have also been described [ 108 ].…”

Section: Gender Differences In Cf and Non-cf Bronchiectasismentioning

confidence: 99%

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Gender differences in bronchiectasis: a real issue?

Vidaillac

Yong

Jaggi

et al. 2018

Breathe

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Gender differences in chronic respiratory disease, including cystic fibrosis and non-cystic fibrosis bronchiectasis are clinically apparent and of increasing importance. Differences in disease prevalence, severity and outcome are all described, however, the precise cause of the gender dichotomy and their associated underlying mechanisms have been poorly characterised. A lack of dedicated clinical and epidemiological research focused in this area has led to a paucity of data and therefore a lack of understanding of its key drivers. Diagnosis, disease pathogenesis and treatment response are all complex but important aspects of bronchiectasis with an evident gender bias. Broadening our understanding of the interplay between microbiology, host physiology and the environment in the context of chronic lung diseases, such as bronchiectasis, is critical to unravelling mechanisms driving the observed gender differences. In this review, epidemiological, biological and environmental evidence related to gender in bronchiectasis is summarised. This illustrates gender differences as a “real issue” with the objective of mapping out a future framework upon which a gender-tailored medical approach may be incorporated into the diagnosis, monitoring and treatment of bronchiectasis.Key pointsCF and non-CF bronchiectasis are complex, multifactorial chronic pulmonary diseases with gender-specific differences in their prevalence, clinical presentation and disease severity.Microbiology and host physiology (immune and inflammatory responses) are essential aspects of bronchiectasis that are influenced by gender.Sex steroid hormones vary in type, fluctuating pattern and concentration throughout life and between the genders with a potential central role in bronchiectasis-related gender differences.Gender-focused clinical and/or therapeutic intervention has the potential to narrow the observed gender gap occurring in bronchiectasis-related lung disease.Educational aimsTo summarise the existing knowledge base of gender-related differences in CF and non-CF bronchiectasis.To highlight key areas of importance in the diagnosis, monitoring and treatment of bronchiectasis that is amenable to clinical and/or pharmacological intervention to narrow the existing “gender gap”.

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Section: Gender Differences In Cf and Non-cf Bronchiectasismentioning

confidence: 99%

Section: Gender Differences In Cf and Non-cf Bronchiectasismentioning

confidence: 99%

Gender differences in bronchiectasis: a real issue?

Vidaillac

Yong

Jaggi

et al. 2018

Breathe

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“…The binding of α-MSH to MC1R receptors induced intracellular signals, primarily elevating intracellular cAMP by adenylate cyclase (Mountjoy et al 1992 ), resulting in the activation of genes involved in melanogenesis. A previous study indicated that the expression of adenylate cyclase was increased by testosterone in rat seminal vesicles (Ramli et al 2016 ). Since finasteride treatment resulted in a decrease of MITF expression (Fig.…”

Section: Resultsmentioning

confidence: 96%

Finasteride inhibits melanogenesis through regulation of the adenylate cyclase in melanocytes and melanoma cells

et al. 2018

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Finasteride is a well-known 5α-reductase inhibitor used for treatment of alopecia and prostate cancer. But the effect of finasteride in regulating melanogenesis is still unclear. In the present study the role of finasteride on melanogenesis was investigated. Finasteride decrease melanin level in melanocyte melan-a cells and B16F10 melanoma cells without inducing cytotoxicity. MC1R (melanocortin 1 receptor) protein expression was also inhibited by finasteride thereby decreasing the expression of adenylate cyclase, MITF (Melanogenesis associated transcription factor), tyrosinases, TRP (tyrosinase-related protein) -1 and -2. Thus our study suggest that finasteride inhibits melanogenesis in melanocyte and melanoma cells by inhibiting MC1R.

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“…In order to examine whether AR signaling was compromised in GCT of p130Cas Δepimouse, we assessed the mRNA levels of several downstream targets of the AR pathway which specifically expressed in GCT cells, such as EGF, NGF, KLK 1 24 , cysteine-rich secretory protein 3 (Crisp 3) 22,25 , prostate transmembrane protein, and androgen-induced 1 (Pmepa 1) 26 , cystic fibrosis transmembrane regulator (Cftr) [27][28][29] , and Runt-related transcription factor 1(Runx 1) 22,30 . A significant reduction in the mRNA levels of these AR-target genes was observed in the SMG from p130Cas Δepimice (Fig.…”

Section: Resultsmentioning

confidence: 99%

p130Cas is required for androgen-dependent postnatal development regulation of submandibular glands

Gao

Fujii

et al. 2023

Sci Rep

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Salivary glands develop through epithelial-mesenchymal interactions and are formed through repeated branching. The Crk-associated substrate protein (p130Cas) serves as an adapter that forms a complex with various proteins via integrin and growth factor signaling, with important regulatory roles in several essential cellular processes. We found that p130Cas is expressed in ductal epithelial cells of the submandibular gland (SMG). We generated epithelial tissue-specific p130Cas-deficient (p130CasΔepi–) mice and aimed to investigate the physiological role of p130Cas in the postnatal development of salivary glands. Histological analysis showed immature development of granular convoluted tubules (GCT) of the SMG in male p130CasΔepi– mice. Immunofluorescence staining showed that nuclear-localized androgen receptors (AR) were specifically decreased in GCT cells in p130CasΔepi– mice. Furthermore, epidermal growth factor-positive secretory granules contained in GCT cells were significantly reduced in p130CasΔepi– mice with downregulated AR signaling. GCTs lacking p130Cas showed reduced numbers and size of secretory granules, disrupted subcellular localization of the cis-Golgi matrix protein GM130, and sparse endoplasmic reticulum membranes in GCT cells. These results suggest that p130Cas plays a crucial role in androgen-dependent GCT development accompanied with ER-Golgi network formation in SMG by regulating the AR signaling.

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Testosterone regulates levels of cystic fibrosis transmembrane regulator, adenylate cyclase, and cAMP in the seminal vesicles of orchidectomized rats

Cited by 11 publications

References 35 publications

Gender differences in bronchiectasis: a real issue?

Gender differences in bronchiectasis: a real issue?

Finasteride inhibits melanogenesis through regulation of the adenylate cyclase in melanocytes and melanoma cells

p130Cas is required for androgen-dependent postnatal development regulation of submandibular glands

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