Human TGF-β3(Transforming Growth Factor Beta 3) ELISA Kit

Name: Human TGF-β3(Transforming Growth Factor Beta 3) ELISA Kit
SKU: DEIA4287
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

Serum, plasma, tissue homogenates and other biological fluids

Species Reactivity

Human

Detection Method

sELISA

Intended Use

TGF-β3 ELISA Kit allows for the in vitro quantitative determination of TGF-β3 concentrations in serum, plasma, tissue homogenates and other biological fluids.

Contents of Kit

Storage

2-8°C for 6 months

Precision

Intra-Assay: CV<8%
Inter-Assay: CV<10%

Detection Range

15.625-1000pg/ml

Sensitivity

< 9.375pg/ml

Standard Curve

Results of a typical standard operation of a TGFβ3 ELISA Kit are listed below. This standard curve was generated at our lab for demonstration purpose only. Users shall obtain standard curve as per experiment by themselves. (N/A=not applicable)

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Transforming Growth Factor Beta 3 Is Required for Excisional Wound Repair In Vivo

PLOS ONE

Authors: Le, Mark; Naridze, Rachelle; Morrison, Jasmine; Biggs, Leah C.; Rhea, Lindsey; Schutte, Brian C.; Kaartinen, Vesa; Dunnwald, Martine

Abstract

Wound healing is a complex process that relies on proper levels of cytokines and growth factors to successfully repair the tissue. Of particular interest are the members of the transforming growth factor family. There are three TGF-beta isoforms-TGF beta 1, 2, and 3, each isoform showing a unique expression pattern, suggesting that they each play a distinct function during development and repair. Previous studies reported an exclusive role for TGF-beta 3 in orofacial development and a potent anti-scarring effect. However, the role of TGF-beta 3 in excisional wound healing and keratinocyte migration remains poorly understood. We tested the effect of TGF-beta 3 levels on excisional cutaneous wounds in the adult mouse by directly injecting recombinant TGF-beta 3 or neutralizing antibody against TGF-beta 3 (NAB) in the wounds. Our results demonstrate that TGF-beta 3 does not promote epithelialization. However, TGF-beta 3 is necessary for wound closure as wounds injected with neutralizing antibody against TGF-beta 3 showed increased epidermal volume and proliferation in conjunction with a delay in keratinocyte migration. Wild type keratinocytes treated with NAB and Tgfb3-deficient keratinocytes closed an in vitro scratch wound with no delay, suggesting that our in vivo observations likely result from a paracrine effect.

Transforming growth factor-beta is involved in maintaining oocyte meiotic arrest by promoting natriuretic peptide type C expression in mouse granulosa cells

CELL DEATH & DISEASE

Authors: Yang, Jing; Zhang, Yu; Xu, Xiaoting; Li, Jia; Yuan, Feifei; Bo, Shumin; Qiao, Jie; Xia, Guoliang; Su, Youqiang; Zhang, Meijia

Abstract

Natriuretic peptide type C (NPPC) secreted by mural granulosa cells (MGCs) maintains oocyte meiotic arrest via the activation of guanylyl cyclase-linked natriuretic peptide receptor 2 (NPR2). Here, we investigated the effect of transforming growth factor (TGF)-beta on NPPC expression in MGCs and oocyte maturation. TGF-beta ligands (TGFB1 and TGFB3, but not TGFB2) and receptors (TGFBR1 and TGFBR2) were predominantly expressed in MGCs. The activation of the follicle-stimulating hormone (FSH) receptor by FSH/equine chorionic gonadotropin (eCG) increased the levels of TGFB1, TGFBR2, and TGF-beta downstream SMAD proteins in MGCs, which were decreased following the activation of the luteinizing hormone (LH) receptor by human chorionic gonadotropin (hCG). TGF-beta significantly increased the gene and protein levels of NPPC in cultured MGCs through SMAD3 binding to Nppc promoter regions. In the presence of FSH, TGF-beta further increased NPPC levels and inhibited oocyte meiotic resumption of cumulus-oocyte complexes (COCs). Moreover, Tgfbr2-specific depletion in granulosa cells using Fshr-Cre mice reduced NPPC mRNA and protein levels, resulting in the weak maintenance of oocyte meiotic arrest within large antral follicles. Tgfbr2 depletion also impaired follicle development, ovulation, and female fertility. Taken together, TGF-beta-promoted NPPC in MGCs is involved in maintaining oocyte meiotic arrest. FSH and LH could regulate NPPC levels in MGCs via TGF-beta and then control the process of oocyte meiosis.