Disease relevance of TGFB3

• Previous immunolocalisation studies of dyschondroplasia have indicated that there is a reduction in the number of growth plate chondrocytes containing the protein transforming growth factor beta 3 (TGF-beta 3) [1].
• Association of INOS, TRAIL, TGF-beta2, TGF-beta3, and IgL genes with response to Salmonella enteritidis in poultry [2].
• The reduction in TGF-beta 3 levels is thought to be associated with the failure of chondrocyte hypertrophy in dyschondroplasia, and provides in vivo evidence that TGF-beta 3 is part of the cascade of events associated with the differentiation of chondrocytes during endochondral ossification in the chick [1].

High impact information on TGFB3

• TGF-beta 2, TGF-beta 3 and the ligand-binding TGF-beta receptor can be detected immunocytochemically in the central retina, a region where apoptosis is most prominent during the early period of PCD [3].
• TGF-beta 3 localization was mainly cytoplasmic in the transitional (early hypertrophic) chondrocytes, but nuclear staining was also detected in some proliferating chondrocytes [4].
• Except for 32 base pairs of identity centered around the TATA box and CRE site and four other relatively small regions of identity, the chicken TGF-beta 3 promoter was found to be structurally very different from the human TGF-beta 3 promoter [5].
• In this study we investigated whether signalling by TGF-beta3 and Wnt-5a cross-talk during chondrogenic differentiation of chick wing mesenchyme [6].
• Inactivation of PKC-alpha and p38 MAPK by specific inhibitors abrogated chondrogenesis stimulated by both TGF-beta3 and Wnt-5a [6].

Biological context of TGFB3

• Significant two-way interactions on antibody response were primarily detected between TGFB3 and TGFB4 genes, and in the lineage of the M15.2 grandsire [7].
• Linkage to the TH locus showed that the TGFB3 locus was physically located on chicken chromosome 5 [8].
• A Msc I restriction fragment length polymorphism (RFLP) marker was used to map the TGFB3 locus to linkage group E7 on the East Lansing reference backcross [8].
• Two regions of sequence homology were detected in the 5'-flanking regions of chicken and human TGF-beta 3 genes: an 86 bp sequence surrounding the major transcription start and a 156 bp sequence in the 5'-untranslated region [9].
• Comparison of 3'-flanking regions of chicken and mammalian TGF-beta 3 genes also revealed conserved sequences [8].

Anatomical context of TGFB3

• Expression of TGF-beta s 2 and 4 mRNAs increased with age, while expression of TGF-beta 3 mRNA was independent of age in chondrocytes cultured from 12- to 17-day-old embryos [10].
• Endoglin is typically located on endothelial cell layers and binds tightly to TGF-beta1 and TGF-beta3 but not well to TGF-beta2 [11].
• In chicken hearts, both transforming growth factor-beta3 (TGF-beta3) and TGF-beta2 are present and have been identified as being important in the production of cushion mesenchyme [11].
• In E11 and older embryos, spinal cord glial or glial progenitor cells, but not neuronal cell bodies were labeled for TGF-beta 3 mRNA [12].
• At embryonic day (E) 3, TGF-beta 3 mRNA as well as TGF-beta 2 and 3 immunoreactivities (IRs) were most prominent in the notochord, wall of the aorta, and dermomyotome [12].

Regulatory relationships of TGFB3

• Overexpression of Wnt-5a or treatment with TGF-beta3 stimulated the activation of protein kinase C-alpha (PKC-alpha) and p38 mitogen-activated protein kinase (MAPK), both positive regulators of chondrogenic differentiation [6].

Other interactions of TGFB3

• These observations suggest that TGF-beta 3 and BMP-2 may be acting in a sequential manner to regulate chick limb mesenchymal cells through the different stages of cartilage differentiation [13].
• The levels of expression of mRNA for GAPDH, TGF-beta 1 and TGF-beta 2 were similar in the two groups, but the expression of TGF-beta 3 mRNA was significantly reduced in the samples from the dyschondroplastic growth plates [1].
• 9. The profile for chicken recombinant latent TGF-beta 3 is slightly shifted with activation between pH 3.1 and 2.5, and between pH 10.0 and 12 [14].

Analytical, diagnostic and therapeutic context of TGFB3

• Immunocytochemistry and western blot analysis indicated that E8 DRG neurons have the TGF-beta receptor type II, and treatment of these cells with NGF induces expression of TGF-beta 3 mRNA [12].
• We have studied the localizations of transforming growth factor-beta (TGF-beta) 2 and 3 immunohistochemically using isoform-specific antibodies and TGF-beta 3 mRNA by in situ hybridization in the nervous system of the 3- to 15-day-old chick embryo with special reference to spinal cord, hindbrain, and dorsal root ganglia (DRG) [12].
• PCR analysis demonstrated TGF beta 2 and TGF beta 3 transcripts in the lens epithelium and fibers throughout pre- and post-hatching development [15].

References