Serum activin A and follistatin concentrations during human pregnancy: a cross-sectional and longitudinal study

O’Connor, Anne E; McFarlane, James R.; Hayward, Susan; Yohkaichiya, Takashi; Groome, Nigel P.; Kretser, David Morritz de

doi:10.1093/humrep/14.3.827

Cited by 115 publications

(72 citation statements)

References 37 publications

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“…Serum samples were assayed against the standard diluted in 5% bovine serum albumin in phosphatebuffered saline (0.01 mol/l). FS concentrations in serum were measured with a radioimmunoassay validated for human FS as previously described (36).…”

Section: Methodsmentioning

confidence: 99%

Serum concentrations of activin and follistatin are elevated and run in parallel in patients with septicemia

Michel

Ebert

Phillips

et al. 2003

European Journal of Endocrinology

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Objective: Activin is a growth and differentiation factor of many cell types, and has recently been implicated in inflammatory processes. Clinical data linking activin and its binding protein, follistatin (FS), are lacking. We measured serum levels of activin and FS in patients diagnosed with septicemia. Patients and measurements: Eight male and seven female patients of different ages, various forms of septicemia and different clinical outcome were investigated and compared with age-and sex-matched healthy controls. Serum concentrations of FS, activin, C-reactive protein (CRP) and blood leukocyte counts were determined during septicemia. Results: The median of the maximum activin concentrations of septicemic patients was 3.9-fold higher than in age-and sex-matched healthy control subjects ðP , 0:01Þ; the median of the maximum FS concentrations was 2.6-fold higher ðP , 0:01Þ: The highest increase of activin in septicemic patients was approximately 15.8-fold, whereas FS increased by up to 13.2-fold above normal. FS, activin and CRP serum levels generally paralleled each other, but were not correlated with leukocyte counts or clinical outcome. Conclusions: Circulatory concentrations of activin and FS are elevated in patients diagnosed with septicemia, consistent with potential roles in the systemic inflammatory response.

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Section: Methodsmentioning

confidence: 99%

Serum concentrations of activin and follistatin are elevated and run in parallel in patients with septicemia

Michel

Ebert

Phillips

et al. 2003

European Journal of Endocrinology

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“…Total protein concentration (mg mL À1 ) was determined using the DC Protein Assay (Bio-Rad Laboratories) according to the manufacturer's instructions. Total FST (bound and unbound) protein was measured from uterine homogenates and serum using a discontinuous RIA (O'Connor et al 1999). Activin A (bA subunit) protein was measured using a commercially available sandwich ELISA (Oxford Bio-Innovations, Cherwell, UK) with some modifications (O'Connor et al 1999).…”

Section: Quantitative Rt-pcr (Qrt-pcr)mentioning

confidence: 99%

“…Total FST (bound and unbound) protein was measured from uterine homogenates and serum using a discontinuous RIA (O'Connor et al 1999). Activin A (bA subunit) protein was measured using a commercially available sandwich ELISA (Oxford Bio-Innovations, Cherwell, UK) with some modifications (O'Connor et al 1999). Uterine and serum FST and activin concentrations (ng mL À1 ) were normalised against total protein, and were expressed as ng of FST or activin A per mg of total protein.…”

Section: Quantitative Rt-pcr (Qrt-pcr)mentioning

confidence: 99%

Follistatin is essential for normal postnatal development and function of mouse oviduct and uterus

Holdsworth-Carson

Craythorn

Winnall

et al. 2015

Reprod. Fertil. Dev.

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Abstract. Female mice lacking the follistatin gene but expressing a human follistatin-315 transgene (tghFST315) have reproductive abnormalities (reduced follicles, no corpora lutea and ovarian-uterine inflammation). We hypothesised that the absence of follistatin-288 causes the abnormal reproductive tract via both developmental abnormalities and abnormal ovarian activity. We characterised the morphology of oviducts and uteri in wild type (WT), tghFST315 and follistatinknockout mice expressing human follistatin-288 (tghFST288). The oviducts and uteri were examined in postnatal Day-0 and adult mice (WT and tghFST315 only) using histology and immunohistochemistry. Adult WT and tghFST315 mice were ovariectomised and treated with vehicle, oestradiol-17b (100 ng injection, dissection 24 h later) or progesterone (1 mg Â three daily injections, dissection 24 h later). No differences were observed in the oviducts or uteri at birth, but abnormalities developed by adulthood. Oviducts of tghFST315 mice failed to coil, the myometrium was disorganised, endometrial gland number was reduced and oviducts and uteri contained abundant leukocytes. After ovariectomy, tghFST315 mice had altered uterine cell proliferation, and inflammation was maintained and exacerbated by oestrogen. These studies show that follistatin is crucial to postnatal oviductal-uterine development and function. Further studies differentiating the role of ovarian versus oviductal-uterine follistatin in reproductive tract function at different developmental stages are warranted.

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“…Conditioned media were obtained from subconfluent R30C cells grown for 72 hours in medium containing 1% FCS. Samples of homogenized tumor extracts and cell culture supernatants were measured in duplicate for total activin A or follistatin concentrations using previously validated immunoassays (28,29).…”

Section: Immunoassays For Follistatin and Activin (Elisa And Ria)mentioning

confidence: 99%

Dissociation of Angiogenesis and Tumorigenesis in Follistatin- and Activin-Expressing Tumors

Krneta¹,

Krøll²,

Alves

et al. 2006

Cancer Research

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The transforming growth factor-B superfamily member activin and its antagonist, follistatin, act as a pleiotropic growth factor system that controls cell proliferation, differentiation, and apoptosis. Activin inhibits fibroblast growth factor 2-induced sprouting angiogenesis in vitro (spheroidal angiogenesis assay) and in vivo (Matrigel assay). To further study the role of the activin/follistatin system during angiogenesis and tumor progression, activin-and follistatin-expressing R30C mammary carcinoma cells were studied in mouse tumor experiments. Surprisingly, activin-expressing tumors grew much faster than follistatin-expressing tumors although they failed to induce increased angiogenesis (as evidenced by low microvessel density counts). Conversely, follistatinexpressing tumors were much smaller but had a dense network of small-diameter capillaries. Qualitative angioarchitectural analyses (mural cell recruitment, perfusion) revealed no major functional differences of the tumor neovasculature. Analysis of activin-and follistatin-expressing R30C cells identified a cell autonomous role of this system in controlling tumor cell growth. Whereas proliferation of R30C cells was not altered, follistatin-expressing R30C cells had an enhanced susceptibility to undergo apoptosis. These findings in experimental tumors are complemented by an intriguing case report of a human renal cell carcinoma that similarly shows a dissociation of angiogenesis and tumorigenesis during tumor progression. Collectively, the data shed further light into the dichotomous stimulating and inhibiting roles that the activin/ follistatin system can exert during angiogenesis and tumor progression. Furthermore, the experiments provide a critical proof-of-principle example for the dissociation of angiogenesis and tumorigenesis, supporting the concept that tumor growth may not be dependent on increased angiogenesis as long as a minimal intratumoral microvessel density is maintained. (Cancer Res 2006; 66(11): 5686-95)

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Serum activin A and follistatin concentrations during human pregnancy: a cross-sectional and longitudinal study

Cited by 115 publications

References 37 publications

Serum concentrations of activin and follistatin are elevated and run in parallel in patients with septicemia

Serum concentrations of activin and follistatin are elevated and run in parallel in patients with septicemia

Follistatin is essential for normal postnatal development and function of mouse oviduct and uterus

Dissociation of Angiogenesis and Tumorigenesis in Follistatin- and Activin-Expressing Tumors

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