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Changes in TGF-beta receptors of rat hepatocytes during primary culture and liver regeneration: increased expression of TGF-beta receptors associated with increased sensitivity to TGF-beta-mediated growth inhibition.
J Cell Physiol. 1998 Sep; 176(3):612-23.JC

Abstract

To clarify the role of transforming growth factor-beta (TGF-beta) and its receptors in hepatocyte growth, we studied the expression of TGF-beta1 and its receptors and the sensitivity to growth inhibition by TGF-beta1 protein in rat hepatocytes derived from resting and regenerating livers. In hepatocytes derived from resting livers, mRNAs for TGF-beta type II receptor (TbetaR-II), insulin-like growth factor-II/mannose 6-phosphate receptor (IGF-II/M-6-PR), and TGF-beta1 increased with time in primary culture. The cell surface TGF-beta receptor proteins (TbetaR-I, II, and III), examined by the receptor affinity-labeling assay using 125I-TGF-beta1, also increased, especially after 48 hr of culture. Hepatocytes were more sensitive to inhibition of DNA synthesis, when the TGF-beta1 protein was added at later times in culture, corresponding to the presence of increased TGF-beta receptors. In hepatocytes from regenerating livers after a partial hepatectomy (PH), an increase of TbetaR-I, TbetaR-II, TbetaR-III, IGF-II/M-6-PR, and TGF-beta1 mRNAs was found, compared with hepatocytes from resting livers. Similarly, using TGF-beta receptor affinity-labeling assay, hepatocytes from PH livers were found to have an increase in TbetaR-I, II, and III proteins, with a peak at 4 days post-PH, compared with hepatocytes from resting livers. When TGF-beta1 protein was added for a short period (6 or 24 hr) after cell attachment to hepatocyte cultures, it inhibited DNA synthesis more effectively in hepatocytes from regenerating compared with resting livers. Our results show that hepatocyte TGF-beta receptors and sensitivity to growth inhibition by TGF-beta1 protein change together and are modulated during liver regeneration, as well as during the conditions of primary culture.

Authors+Show Affiliations

Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pennsylvania 15213, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9699514

Citation

Nishikawa, Y, et al. "Changes in TGF-beta Receptors of Rat Hepatocytes During Primary Culture and Liver Regeneration: Increased Expression of TGF-beta Receptors Associated With Increased Sensitivity to TGF-beta-mediated Growth Inhibition." Journal of Cellular Physiology, vol. 176, no. 3, 1998, pp. 612-23.
Nishikawa Y, Wang M, Carr BI. Changes in TGF-beta receptors of rat hepatocytes during primary culture and liver regeneration: increased expression of TGF-beta receptors associated with increased sensitivity to TGF-beta-mediated growth inhibition. J Cell Physiol. 1998;176(3):612-23.
Nishikawa, Y., Wang, M., & Carr, B. I. (1998). Changes in TGF-beta receptors of rat hepatocytes during primary culture and liver regeneration: increased expression of TGF-beta receptors associated with increased sensitivity to TGF-beta-mediated growth inhibition. Journal of Cellular Physiology, 176(3), 612-23.
Nishikawa Y, Wang M, Carr BI. Changes in TGF-beta Receptors of Rat Hepatocytes During Primary Culture and Liver Regeneration: Increased Expression of TGF-beta Receptors Associated With Increased Sensitivity to TGF-beta-mediated Growth Inhibition. J Cell Physiol. 1998;176(3):612-23. PubMed PMID: 9699514.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Changes in TGF-beta receptors of rat hepatocytes during primary culture and liver regeneration: increased expression of TGF-beta receptors associated with increased sensitivity to TGF-beta-mediated growth inhibition. AU - Nishikawa,Y, AU - Wang,M, AU - Carr,B I, PY - 1998/8/12/pubmed PY - 2000/6/20/medline PY - 1998/8/12/entrez SP - 612 EP - 23 JF - Journal of cellular physiology JO - J Cell Physiol VL - 176 IS - 3 N2 - To clarify the role of transforming growth factor-beta (TGF-beta) and its receptors in hepatocyte growth, we studied the expression of TGF-beta1 and its receptors and the sensitivity to growth inhibition by TGF-beta1 protein in rat hepatocytes derived from resting and regenerating livers. In hepatocytes derived from resting livers, mRNAs for TGF-beta type II receptor (TbetaR-II), insulin-like growth factor-II/mannose 6-phosphate receptor (IGF-II/M-6-PR), and TGF-beta1 increased with time in primary culture. The cell surface TGF-beta receptor proteins (TbetaR-I, II, and III), examined by the receptor affinity-labeling assay using 125I-TGF-beta1, also increased, especially after 48 hr of culture. Hepatocytes were more sensitive to inhibition of DNA synthesis, when the TGF-beta1 protein was added at later times in culture, corresponding to the presence of increased TGF-beta receptors. In hepatocytes from regenerating livers after a partial hepatectomy (PH), an increase of TbetaR-I, TbetaR-II, TbetaR-III, IGF-II/M-6-PR, and TGF-beta1 mRNAs was found, compared with hepatocytes from resting livers. Similarly, using TGF-beta receptor affinity-labeling assay, hepatocytes from PH livers were found to have an increase in TbetaR-I, II, and III proteins, with a peak at 4 days post-PH, compared with hepatocytes from resting livers. When TGF-beta1 protein was added for a short period (6 or 24 hr) after cell attachment to hepatocyte cultures, it inhibited DNA synthesis more effectively in hepatocytes from regenerating compared with resting livers. Our results show that hepatocyte TGF-beta receptors and sensitivity to growth inhibition by TGF-beta1 protein change together and are modulated during liver regeneration, as well as during the conditions of primary culture. SN - 0021-9541 UR - https://www.unboundmedicine.com/medline/citation/9699514/Changes_in_TGF_beta_receptors_of_rat_hepatocytes_during_primary_culture_and_liver_regeneration:_increased_expression_of_TGF_beta_receptors_associated_with_increased_sensitivity_to_TGF_beta_mediated_growth_inhibition_ L2 - https://doi.org/10.1002/(SICI)1097-4652(199809)176:3<612::AID-JCP18>3.0.CO;2-0 DB - PRIME DP - Unbound Medicine ER -