scholarly journals Expression of transforming growth factor-β isoforms and their receptors in utero-vaginal junction of hen oviduct in presence or absence of resident sperm with reference to sperm storage

Reproduction ◽  
2006 ◽  
Vol 132 (5) ◽  
pp. 781-790 ◽  
Author(s):  
Shubash Chandra Das ◽  
Naoki Isobe ◽  
Masahide Nishibori ◽  
Yukinori Yoshimura
Keyword(s):  
Growth Factor ◽  
Western Blot ◽  
Reverse Transcriptase ◽  
Mrna Expression ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
In Utero ◽  
Sperm Storage ◽  
Reverse Transcriptase Pcr ◽  
Sperm Storage Tubules

Our goal was to determine whether transforming growth factor β (TGFβ) isoforms were involved in the process of sperm survivability in the sperm-storage tubules (SST) in the utero-vaginal junction (UVJ) of hen oviduct. The birds were artificially inseminated. The mRNA expressions of three types of TGFβ isoforms (TGFβ2, TGFβ3, and TGFβ4) and three types of receptors (TβR1, TβR2, and TβR3) were examined in the presence or in the absence of resident sperm in SST by semi-quantitative reverse transcriptase-PCR. The mRNA expression of TGFβs and TβRs in sperm was also examined. Immunocytochemistry and western blot were performed for TβR2 to confirm its localization in UVJ. The sperm were observed at least 10 days after insemination by histology. The mRNA expressions of TGFβs and TβRs were significantly increased in UVJ in the presence of resident sperm in SST. The mRNA expressions of TGFβs and TβRs were also observed in sperm. Immunohistochemistry revealed that TβR2 were located in lymphocytes in UVJ and SST cells. The presence of TβR2 in UVJ was also confirmed by western blot. These results suggest that enhanced expressions of TGFβs and TβRs in UVJ may protect sperm in SST, probably by suppressing anti-sperm immunoreactions.

scholarly journals Transient changes of transforming growth factor-β expression in the small intestine of the pig in association with weaning

2005 ◽  
Vol 93 (1) ◽  
pp. 37-45 ◽  
Author(s):  
Jie Mei ◽  
Ruo-Jun Xu
Keyword(s):  
Small Intestine ◽  
Growth Factor ◽  
Western Blot ◽  
Intestinal Mucosa ◽  
Blot Analysis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Intestinal Villus ◽  
Weaning Pigs ◽  
Tgf Β1

It is well known that early weaning causes marked changes in intestinal structure and function, and transforming growth factor-β (TGF-β) is believed to play an important regulatory role in post-weaning adaptation of the small intestine. The present study examined the distribution and expression intensity of TGF-β in the small intestinal mucosa of pre- and post-weaning pigs using a specific immunostaining technique and Western blot analysis. The level of TGF-β in the intestinal mucosa, as estimated by Western blot analysis, did not change significantly during weaning. However, when examined by the immunostaining technique, TGF-β1 (one of the TGF-β isoforms dominantly expressed in the tissue) at the intestinal villus epithelium, particularly at the apical membrane of the epithelium, decreased significantly 4 d after weaning, while the staining intensity increased significantly at the intestinal crypts compared with that in pre-weaning pigs. These changes were transient, with the immunostaining intensity for TGF-β1 at the intestinal villi and the crypts returning to the pre-weaning level by 8 d post-weaning. The transient decrease in TGF-β1 level at the intestinal villus epithelium was associated with obvious intestinal villus atrophy and marked reduction of mucosal digestive enzyme activities. Furthermore, the number of leucocytes staining positively for TGF-β1 increased significantly in the pig intestinal lamina propria 4 d after weaning. These findings strongly suggest that TGF-β plays an important role in the post-weaning adaptation process in the intestine of the pig.

scholarly journals Latency-Associated Peptide of Transforming Growth Factor β Enhances Mycobacteriocidal Immunity in the Lung duringMycobacterium bovis BCG Infection in C57BL/6 Mice

2000 ◽  
Vol 68 (11) ◽  
pp. 6505-6508 ◽  
Author(s):  
K. A. Wilkinson ◽  
T. D. Martin ◽  
S. M. Reba ◽  
H. Aung ◽  
R. W. Redline ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Growth Factor ◽  
Mrna Expression ◽  
Mycobacterium Bovis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Gamma Interferon ◽  
T Cell Proliferation

ABSTRACT Latency-associated peptide of transforming growth factor β (TGF-β) (LAP) was used to determine whether in vivo modulation of TGF-β bioactivity enhanced pulmonary immunity to Mycobacterium bovis BCG infection in C57BL/6 mice. LAP decreased BCG growth in the lung and enhanced antigen-specific T-cell proliferation and gamma interferon mRNA expression. Thus, susceptibility of the lung to primary BCG infection may be partially mediated by the immunosuppressive effects of TGF-β.

Activation of elastin transcription by transforming growth factor-β in human lung fibroblasts

2007 ◽  
Vol 292 (4) ◽  
pp. L944-L952 ◽  
Author(s):  
Ping-Ping Kuang ◽  
Xiao-Hui Zhang ◽  
Celeste B. Rich ◽  
Judith A. Foster ◽  
Mangalalaxmy Subramanian ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Lung Fibroblasts ◽  
Mrna Levels ◽  
Phosphatidylinositol 3 Kinase ◽  
Akt Phosphorylation ◽  
Mapk Inhibitor ◽  
Phosphatidylinositol 3

Elastin synthesis is essential for lung development and postnatal maturation as well as for repair following injury. Using human embryonic lung fibroblasts that express undetectable levels of elastin as assessed by Northern analyses, we found that treatment with exogenous transforming growth factor-β (TGF-β) induced rapid and transient increases in levels of elastin heterogeneous nuclear RNA (hnRNA) followed by increases of elastin mRNA and protein expression. In fibroblasts derived from transgenic mice, TGF-β induced increases in the expression of a human elastin gene promoter fragment driving a chloramphenicol acetyl transferase reporter gene. The induction of elastin hnRNA and mRNA expression by TGF-β was abolished by pretreatments with TGF-β receptor I inhibitor, global transcription inhibitor actinomycin D, and partially blocked by addition of protein synthesis inhibitor cycloheximide, but was not affected by the p44/42 MAPK inhibitor U0126. Pretreatment with the p38 MAPK inhibitor SB-203580 also partially attenuated the levels of TGF-β-induced elastin mRNA but not its hnRNA. Western analysis indicated that TGF-β stimulated Akt phosphorylation. Inhibition of phosphatidylinositol 3-kinase and Akt phosphorylation by LY-294002 abolished TGF-β-induced increases in elastin hnRNA and mRNA expression. Treatment of lung fibroblasts with interleukin-1β or the histone deacetylase inhibitor trichostatin A inhibited TGF-β-induced elastin mRNA and hnRNA expression by a mechanism that involved inhibition of Akt phosphorylation. Downregulation of Akt2 but not Akt1 expression employing small interfering RNA duplexes blocked TGF-β-induced increases of elastin hnRNA and mRNA levels. Together, our results demonstrated that TGF-β activates elastin transcription that is dependent on phosphatidylinositol 3-kinase/Akt activity.

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