Angiotensin II induces apoptosis in human mural granulosa-lutein cells, but not in cumulus cells

FSH receptor, KL1/2, P450, and PAPP genes in granulosa-lutein cells from in vitro fertilization patients show a different expression pattern depending on the infertility diagnosis

“…to regulate steroidogenesis (36)(37)(38). The expression of OVRAS is altered in women with PCOS: further work may elucidate the interaction between OVRAS and the KL1/ KL2 system in healthy and diseased ovaries.…”

Expression of angiotensin II type 1 (AT1) and angiotensin II type 2 (AT2) receptors in human granulosa-lutein (GL) cells: correlation with infertility diagnoses

“…We have previously shown that AngII causes GL cell apoptosis, preferentially via the AT2 receptor (29), and that increased GL cell apoptosis is associated with increased embryo fragmentation (28). The AT1 receptor promotes generalized positive effects in growth and development, in general, antiapoptotic effects.…”

“…Granulosa-lutein cells were collected from FF obtained during ultrasound-guided transvaginal oocyte retrieval and purified as previously described (28)(29) immediately after egg retrieval. Briefly, all FF from each patient was pooled and the GL cells lightly centrifuged after removal of the oocyte.…”

“…However, gonadotropin-stimulated mural GL cells obtained from the FF of women at the time of egg retrieval for IVF undergo apoptosis (22)(23)(24)(25)(26)(27), raising the possibility that the gonadotropin-driven OVRAS is involved in follicle cell dynamics and has a relationship with the developing oocyte. We demonstrated that GL cells undergo different degrees of apoptosis as a function of patients' age (younger < older) and IVF outcome (unsuccessful > successful pregnancy) (28) and that AngII induces in vitro apoptosis of gonadotropin-exposed human IVF GL cells but not of cumulus cells, a mechanism which seems to be preferentially modulated by the AT2 receptor (29).…”

Therapeutic inhibition of the renin angiotensin aldosterone system

“…The principal concern with ARB pharmacology is that blockade of the AII AT1 receptor will favour activity at the unblocked AT2 receptor (and other AII receptors). Although this may be considered as a desirable side effect, given the vasodilator and antiproliferative profile of cellular activities linked to AT2 receptor stimulation, other tissue responses such as apoptosis and pro-inflammatory effects give pause for thought, especially in chronic ARB use [54][55][56][57][58]. And as with ACE inhibition, AII AT1 receptor antagonism leads to an increase in renin and AII levels as a consequence of interrupted negative feedback on renin release.…”