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Expression of angiotensin II type 1 receptor-interacting molecule in normal human kidney and IgA nephropathy.
Am J Physiol Renal Physiol. 2010 Oct; 299(4):F720-31.AJ

Abstract

The intrarenal renin-angiotensin system plays a crucial role in the regulation of renal circulation and sodium reabsorption through the activation of vascular, glomerular, and tubular angiotensin II type 1 (AT(1)) receptor signaling. We previously cloned a molecule that specifically interacted with the murine AT(1) receptor to inhibit AT(1) receptor signaling, which we named ATRAP (for AT(1) receptor-associated protein). Since murine ATRAP was shown to be highly expressed in the kidney, in the present study we investigated expression and distribution of human ATRAP in normal kidney and renal biopsy specimens from patients with IgA nephropathy. In the normal human kidney, both ATRAP mRNA and protein were widely and abundantly distributed along the renal tubules from Bowman's capsule to the medullary collecting ducts. In all renal tubular epithelial cells, the ATRAP protein colocalized with the AT(1) receptor. In renal biopsy specimens with IgA nephropathy, a significant positive correlation between ATRAP and AT(1) receptor gene expression was observed. There was also a positive relationship between tubulointerstitial ATRAP expression and the estimated glomerular filtration rate in patients with IgA nephropathy. Furthermore, we examined the function of the tubular AT(1) receptor using an immortalized cell line of mouse distal convoluted tubule cells (mDCT) and found that overexpression of ATRAP by adenoviral gene transfer suppressed the angiotensin II-mediated increases in transforming growth factor-β production in mDCT cells. These findings suggest that ATRAP might play a role in balancing the renal renin-angiotensin system synergistically with the AT(1) receptor by counterregulatory effects in IgA nephropathy and propose an antagonistic effect of tubular ATRAP on AT(1) receptor signaling.

Authors+Show Affiliations

Dept. of Medical Science and Cardiorenal Medicine, Yokohama City Univ. Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20685825

Citation

Masuda, Shin-ichiro, et al. "Expression of Angiotensin II Type 1 Receptor-interacting Molecule in Normal Human Kidney and IgA Nephropathy." American Journal of Physiology. Renal Physiology, vol. 299, no. 4, 2010, pp. F720-31.
Masuda S, Tamura K, Wakui H, et al. Expression of angiotensin II type 1 receptor-interacting molecule in normal human kidney and IgA nephropathy. Am J Physiol Renal Physiol. 2010;299(4):F720-31.
Masuda, S., Tamura, K., Wakui, H., Maeda, A., Dejima, T., Hirose, T., Toyoda, M., Azuma, K., Ohsawa, M., Kanaoka, T., Yanagi, M., Yoshida, S., Mitsuhashi, H., Matsuda, M., Ishigami, T., Toya, Y., Suzuki, D., Nagashima, Y., & Umemura, S. (2010). Expression of angiotensin II type 1 receptor-interacting molecule in normal human kidney and IgA nephropathy. American Journal of Physiology. Renal Physiology, 299(4), F720-31. https://doi.org/10.1152/ajprenal.00667.2009
Masuda S, et al. Expression of Angiotensin II Type 1 Receptor-interacting Molecule in Normal Human Kidney and IgA Nephropathy. Am J Physiol Renal Physiol. 2010;299(4):F720-31. PubMed PMID: 20685825.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Expression of angiotensin II type 1 receptor-interacting molecule in normal human kidney and IgA nephropathy. AU - Masuda,Shin-ichiro, AU - Tamura,Kouichi, AU - Wakui,Hiromichi, AU - Maeda,Akinobu, AU - Dejima,Toru, AU - Hirose,Tomonori, AU - Toyoda,Masao, AU - Azuma,Koichi, AU - Ohsawa,Masato, AU - Kanaoka,Tomohiko, AU - Yanagi,Mai, AU - Yoshida,Shin-ichiro, AU - Mitsuhashi,Hiroshi, AU - Matsuda,Miyuki, AU - Ishigami,Tomoaki, AU - Toya,Yoshiyuki, AU - Suzuki,Daisuke, AU - Nagashima,Yoji, AU - Umemura,Satoshi, Y1 - 2010/08/04/ PY - 2010/8/6/entrez PY - 2010/8/6/pubmed PY - 2010/10/27/medline SP - F720 EP - 31 JF - American journal of physiology. Renal physiology JO - Am. J. Physiol. Renal Physiol. VL - 299 IS - 4 N2 - The intrarenal renin-angiotensin system plays a crucial role in the regulation of renal circulation and sodium reabsorption through the activation of vascular, glomerular, and tubular angiotensin II type 1 (AT(1)) receptor signaling. We previously cloned a molecule that specifically interacted with the murine AT(1) receptor to inhibit AT(1) receptor signaling, which we named ATRAP (for AT(1) receptor-associated protein). Since murine ATRAP was shown to be highly expressed in the kidney, in the present study we investigated expression and distribution of human ATRAP in normal kidney and renal biopsy specimens from patients with IgA nephropathy. In the normal human kidney, both ATRAP mRNA and protein were widely and abundantly distributed along the renal tubules from Bowman's capsule to the medullary collecting ducts. In all renal tubular epithelial cells, the ATRAP protein colocalized with the AT(1) receptor. In renal biopsy specimens with IgA nephropathy, a significant positive correlation between ATRAP and AT(1) receptor gene expression was observed. There was also a positive relationship between tubulointerstitial ATRAP expression and the estimated glomerular filtration rate in patients with IgA nephropathy. Furthermore, we examined the function of the tubular AT(1) receptor using an immortalized cell line of mouse distal convoluted tubule cells (mDCT) and found that overexpression of ATRAP by adenoviral gene transfer suppressed the angiotensin II-mediated increases in transforming growth factor-β production in mDCT cells. These findings suggest that ATRAP might play a role in balancing the renal renin-angiotensin system synergistically with the AT(1) receptor by counterregulatory effects in IgA nephropathy and propose an antagonistic effect of tubular ATRAP on AT(1) receptor signaling. SN - 1522-1466 UR - https://www.unboundmedicine.com/medline/citation/20685825/Expression_of_angiotensin_II_type_1_receptor_interacting_molecule_in_normal_human_kidney_and_IgA_nephropathy_ L2 - http://www.physiology.org/doi/full/10.1152/ajprenal.00667.2009?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -