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1,25-(OH(2))D(3) alters the transforming growth factor beta signaling pathway in renal tissue.
J Surg Res 2001; 100(2):171-5JS

Abstract

BACKGROUND

1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) plays an important role in regulating immune responses, in addition to its effects on bone metabolism. The cytokine transforming growth factor beta (TGF-beta) regulates diverse biological processes, including cellular proliferation and differentiation, immune modulation, and modulation of extracellular matrix deposition. 1,25-(OH)(2)D(3) interacts in vitro with Smad proteins, important regulators of TGF-beta signal transduction. We hypothesized that exogenous 1,25-(OH)(2)D(3) would alter levels of TGF-beta(1) and TGF-beta(1) signaling proteins in renal tissue.

METHODS

C57BL6 mice and Lewis rats were placed on diets with or without 1,25-(OH)(2)D(3) for 14 days. Renal lysates were examined for TGF-beta(1), vitamin D receptor (VDR), and Smad3 protein levels using a cell proliferation assay and Western blot analysis. Coimmunoprecipitation was used to determine if any interaction between VDR and Smad3 proteins occurs in vivo. Reverse transcription-polymerase chain reaction (RT-PCR) was used to assess messenger RNA (mRNA) levels for all of these molecules.

RESULTS

Vitamin D supplementation decreased VDR and Smad3 protein levels. Coimmunoprecipitation of VDR and Smad3 revealed a Smad3-VDR interaction in vivo. Vitamin D-treated rats had a significant (P = 0.001) reduction in bioactive renal TGF-beta(1). RT-PCR demonstrated no difference in mRNA expression for either VDR or TGF-beta(1).

CONCLUSION

Our results suggest that vitamin D has a significant effect in regulating levels of bioactive TGF-beta(1) and appears to affect aspects of the TGF-beta(1) signaling system. These effects, in combination with the immunomodulatory actions of vitamin D, may alter the evolution of chronic rejection in renal transplants.

Authors+Show Affiliations

Department of Surgery, University of Wisconsin, 600 Highland Avenue, Madison, WI 53792, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11592788

Citation

Aschenbrenner, J K., et al. "1,25-(OH(2))D(3) Alters the Transforming Growth Factor Beta Signaling Pathway in Renal Tissue." The Journal of Surgical Research, vol. 100, no. 2, 2001, pp. 171-5.
Aschenbrenner JK, Sollinger HW, Becker BN, et al. 1,25-(OH(2))D(3) alters the transforming growth factor beta signaling pathway in renal tissue. J Surg Res. 2001;100(2):171-5.
Aschenbrenner, J. K., Sollinger, H. W., Becker, B. N., & Hullett, D. A. (2001). 1,25-(OH(2))D(3) alters the transforming growth factor beta signaling pathway in renal tissue. The Journal of Surgical Research, 100(2), pp. 171-5.
Aschenbrenner JK, et al. 1,25-(OH(2))D(3) Alters the Transforming Growth Factor Beta Signaling Pathway in Renal Tissue. J Surg Res. 2001;100(2):171-5. PubMed PMID: 11592788.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 1,25-(OH(2))D(3) alters the transforming growth factor beta signaling pathway in renal tissue. AU - Aschenbrenner,J K, AU - Sollinger,H W, AU - Becker,B N, AU - Hullett,D A, PY - 2001/10/11/pubmed PY - 2002/1/5/medline PY - 2001/10/11/entrez SP - 171 EP - 5 JF - The Journal of surgical research JO - J. Surg. Res. VL - 100 IS - 2 N2 - BACKGROUND: 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) plays an important role in regulating immune responses, in addition to its effects on bone metabolism. The cytokine transforming growth factor beta (TGF-beta) regulates diverse biological processes, including cellular proliferation and differentiation, immune modulation, and modulation of extracellular matrix deposition. 1,25-(OH)(2)D(3) interacts in vitro with Smad proteins, important regulators of TGF-beta signal transduction. We hypothesized that exogenous 1,25-(OH)(2)D(3) would alter levels of TGF-beta(1) and TGF-beta(1) signaling proteins in renal tissue. METHODS: C57BL6 mice and Lewis rats were placed on diets with or without 1,25-(OH)(2)D(3) for 14 days. Renal lysates were examined for TGF-beta(1), vitamin D receptor (VDR), and Smad3 protein levels using a cell proliferation assay and Western blot analysis. Coimmunoprecipitation was used to determine if any interaction between VDR and Smad3 proteins occurs in vivo. Reverse transcription-polymerase chain reaction (RT-PCR) was used to assess messenger RNA (mRNA) levels for all of these molecules. RESULTS: Vitamin D supplementation decreased VDR and Smad3 protein levels. Coimmunoprecipitation of VDR and Smad3 revealed a Smad3-VDR interaction in vivo. Vitamin D-treated rats had a significant (P = 0.001) reduction in bioactive renal TGF-beta(1). RT-PCR demonstrated no difference in mRNA expression for either VDR or TGF-beta(1). CONCLUSION: Our results suggest that vitamin D has a significant effect in regulating levels of bioactive TGF-beta(1) and appears to affect aspects of the TGF-beta(1) signaling system. These effects, in combination with the immunomodulatory actions of vitamin D, may alter the evolution of chronic rejection in renal transplants. SN - 0022-4804 UR - https://www.unboundmedicine.com/medline/citation/11592788/125__OH_2__D_3__alters_the_transforming_growth_factor_beta_signaling_pathway_in_renal_tissue_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-4804(01)96221-3 DB - PRIME DP - Unbound Medicine ER -