Matches in SemOpenAlex for { <https://semopenalex.org/work/W2131608742> ?p ?o ?g. }
- W2131608742 endingPage "23" @default.
- W2131608742 startingPage "15" @default.
- W2131608742 abstract "Sex steroids are important regulators for longitudinal growth, bone mass accrual, and sexual dimorphism of the skeleton. 17β-Estradiol regulates proliferation and differentiation of female chondrocytes via a membrane-associated signaling pathway in addition to its estrogen receptor (ER) mediated effects. In contrast, testosterone does not elicit a similar membrane response, either in male or female cells. Whereas female rat growth plate chondrocytes convert testosterone to 17β-estradiol, male chondrocytes produce 5α-dihydrotestosterone (DHT). Previously DHT was found to mediate sex-specific effects of testosterone in male cells, but it is not known if a membrane-signaling pathway is involved. In this study, we hypothesized that DHT can induce sex-specific rapid membrane effects similar to other steroid hormones. Confluent cultures of chondrocytes isolated from resting zones of growth plates of both male and female rats were treated with 10(-10)-10(-7)M testosterone or DHT for 3, 9, 90 and 270min and protein kinase C (PKC) and phospholipase A2 (PLA2) activities were measured. To examine potential signaling pathways involved in PKC activation, male chondrocytes were treated with 10(-7)M DHT for 9min in the presence or absence of the phospholipase C (PLC) inhibitor U73122, the secretory PLA2 inhibitor quinacrine or the cytosolic PLA2 inhibitor AACOCF3; the Gαi inhibitor pertussis toxin (PTX) or Gαs activator cholera toxin (CTX), and the general G-protein inhibitor GDPβS; thapsigargin, an inhibitor of a Ca-ATPase pump in the endoplasmic reticulum; verapamil and nifedipine, inhibitors of specific L type Ca2+ channels on the cell membrane; and cyproterone acetate (CPA), which is an inhibitor of the classical androgen receptor (AR); as well as the transcription inhibitor actinomycin D, or the translation inhibitor cycloheximide. DHT induced a dose-dependent increase in PKC and PLA2 activity in male cells with the highest increase at 10(-7)M DHT (p<0.05), whereas testosterone had no effect. PKC activity was augmented at 9 and 90 min, and then decreased to baseline at 270min. Neither testosterone nor DHT affected PKC in female cells. U73122, quinacrine, and AACOCF3 inhibited DHT-induced activation of PKC. DHT treatment for 9 min had no effect in [(3)H]-thymidine incorporation in quiescent confluent cultures but caused a dose dependent increase in alkaline phosphatase specific activity. Inhibition of PLC reduced the response of to DHT in a dose dependent manner, indicating that PLC is involved. In conclusion, our study indicates that DHT, but not testosterone, has sex-specific rapid membrane effects in male growth plate chondrocytes involving PLC and PLA2-mediated PKC signaling pathways. Together with previous observations showing that male cells convert testosterone to DHT, these results suggest that DHT might act in the membrane through an autocrine/paracrine mechanism." @default.
- W2131608742 created "2016-06-24" @default.
- W2131608742 creator A5029880479 @default.
- W2131608742 creator A5037015805 @default.
- W2131608742 creator A5052368052 @default.
- W2131608742 creator A5066141929 @default.
- W2131608742 date "2012-10-01" @default.
- W2131608742 modified "2023-09-26" @default.
- W2131608742 title "Rapid membrane responses to dihydrotestosterone are sex dependent in growth plate chondrocytes" @default.
- W2131608742 cites W1486711418 @default.
- W2131608742 cites W148785554 @default.
- W2131608742 cites W1518728605 @default.
- W2131608742 cites W1545591640 @default.
- W2131608742 cites W1548293202 @default.
- W2131608742 cites W1573258040 @default.
- W2131608742 cites W1593385535 @default.
- W2131608742 cites W1754858407 @default.
- W2131608742 cites W1970792195 @default.
- W2131608742 cites W1972415345 @default.
- W2131608742 cites W1972664132 @default.
- W2131608742 cites W1974968903 @default.
- W2131608742 cites W1980224338 @default.
- W2131608742 cites W1981350213 @default.
- W2131608742 cites W1984087728 @default.
- W2131608742 cites W1990367576 @default.
- W2131608742 cites W1993670763 @default.
- W2131608742 cites W1999566158 @default.
- W2131608742 cites W2001303891 @default.
- W2131608742 cites W2006893504 @default.
- W2131608742 cites W2008052643 @default.
- W2131608742 cites W2011203985 @default.
- W2131608742 cites W2013034768 @default.
- W2131608742 cites W2019269074 @default.
- W2131608742 cites W2024296404 @default.
- W2131608742 cites W2024566047 @default.
- W2131608742 cites W2026135073 @default.
- W2131608742 cites W2030464593 @default.
- W2131608742 cites W2038027940 @default.
- W2131608742 cites W2043390449 @default.
- W2131608742 cites W2053617528 @default.
- W2131608742 cites W2055828189 @default.
- W2131608742 cites W2059939225 @default.
- W2131608742 cites W2061528650 @default.
- W2131608742 cites W2066570340 @default.
- W2131608742 cites W2077936658 @default.
- W2131608742 cites W2078280901 @default.
- W2131608742 cites W2083517169 @default.
- W2131608742 cites W2109306505 @default.
- W2131608742 cites W2113893197 @default.
- W2131608742 cites W2132487460 @default.
- W2131608742 cites W2134223482 @default.
- W2131608742 cites W2137889099 @default.
- W2131608742 cites W2140697327 @default.
- W2131608742 cites W2146352944 @default.
- W2131608742 cites W2147881577 @default.
- W2131608742 cites W2154818098 @default.
- W2131608742 cites W2156506178 @default.
- W2131608742 cites W2164934600 @default.
- W2131608742 cites W2188249594 @default.
- W2131608742 cites W3021926250 @default.
- W2131608742 cites W4232534952 @default.
- W2131608742 cites W4239099866 @default.
- W2131608742 cites W4243952167 @default.
- W2131608742 cites W4244024000 @default.
- W2131608742 cites W4251011603 @default.
- W2131608742 doi "https://doi.org/10.1016/j.jsbmb.2011.12.009" @default.
- W2131608742 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22207084" @default.
- W2131608742 hasPublicationYear "2012" @default.
- W2131608742 type Work @default.
- W2131608742 sameAs 2131608742 @default.
- W2131608742 citedByCount "15" @default.
- W2131608742 countsByYear W21316087422012 @default.
- W2131608742 countsByYear W21316087422013 @default.
- W2131608742 countsByYear W21316087422014 @default.
- W2131608742 countsByYear W21316087422015 @default.
- W2131608742 countsByYear W21316087422016 @default.
- W2131608742 countsByYear W21316087422020 @default.
- W2131608742 countsByYear W21316087422021 @default.
- W2131608742 crossrefType "journal-article" @default.
- W2131608742 hasAuthorship W2131608742A5029880479 @default.
- W2131608742 hasAuthorship W2131608742A5037015805 @default.
- W2131608742 hasAuthorship W2131608742A5052368052 @default.
- W2131608742 hasAuthorship W2131608742A5066141929 @default.
- W2131608742 hasConcept C126322002 @default.
- W2131608742 hasConcept C134018914 @default.
- W2131608742 hasConcept C181199279 @default.
- W2131608742 hasConcept C195794163 @default.
- W2131608742 hasConcept C2776551241 @default.
- W2131608742 hasConcept C2777006276 @default.
- W2131608742 hasConcept C2777911890 @default.
- W2131608742 hasConcept C2778597717 @default.
- W2131608742 hasConcept C2779881493 @default.
- W2131608742 hasConcept C55493867 @default.
- W2131608742 hasConcept C62478195 @default.
- W2131608742 hasConcept C71315377 @default.
- W2131608742 hasConcept C71924100 @default.
- W2131608742 hasConcept C86803240 @default.
- W2131608742 hasConcept C95444343 @default.