AT1 expression in human urethral stricture tissue

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Abstract

Background

Urethral stricture has a high recurrence rate. There is a common doctrine stating that “once a stricture, always a stricture”. This fibrotic disease pathophysiology, pathologically characterized by excessive production, deposition and contraction of extracellular matrix is unknown. Angiotensin II type 1 (AT ₁) receptor primarily induces angiogenesis, cellular proliferation and inflammatory responses. AT ₁ receptors are also expressed in the fibroblasts of hypertrophic scars, whereas angiotensin II (AngII) regulates DNA synthesis in hypertrophic scar fibroblasts through a negative cross talk between AT ₁ and angiotensin II type 2 (AT ₂) receptors, which might contribute to the formation and maturation of human hypertrophic scars.

Objective

This study was conducted to determine the expression of AT ₁ receptors in urethral stricture tissues.

Methods

Urethral stricture tissues were collected from patients during anastomotic urethroplasty surgery. There were 24 tissue samples collected in this study with 2 samples of normal urethra for the control group. Immunohistochemistry study was performed to detect the presence of AT ₁ receptor expression. Data were analyzed using Mann–Whitney U test, and statistical analysis was performed with SPSS version 20.

Results

This study showed that positive staining of AT ₁ receptor was found in all urethral stricture tissues (n=24). A total of 8.33% patients had low intensity, 41.67% had moderate intensity and 50% had high intensity of AT ₁ receptors, while in the control group, 100% patients had no intensity of AT ₁ receptors. Using the Mann–Whitney U test, it was found that urethral stricture tissue had a higher intensity of AT ₁ receptors than normal urethral tissue with a p-value = 0.012.

Conclusion

The results showed that AT ₁ receptor had a higher intensity in the urethral stricture tissue and that AT ₁ receptor may play an important role in the development of urethral stricture.

Related collections

Most cited references 27

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In recent years, the focus of interest on the role of the renin-angiotensin system (RAS) in the pathophysiology of hypertension and organ injury has changed to a major emphasis on the role of the local RAS in specific tissues. In the kidney, all of the RAS components are present and intrarenal angiotensin II (Ang II) is formed by independent multiple mechanisms. Proximal tubular angiotensinogen, collecting duct renin, and tubular angiotensin II type 1 (AT1) receptors are positively augmented by intrarenal Ang II. In addition to the classic RAS pathways, prorenin receptors and chymase are also involved in local Ang II formation in the kidney. Moreover, circulating Ang II is actively internalized into proximal tubular cells by AT1 receptor-dependent mechanisms. Consequently, Ang II is compartmentalized in the renal interstitial fluid and the proximal tubular compartments with much higher concentrations than those existing in the circulation. Recent evidence has also revealed that inappropriate activation of the intrarenal RAS is an important contributor to the pathogenesis of hypertension and renal injury. Thus, it is necessary to understand the mechanisms responsible for independent regulation of the intrarenal RAS. In this review, we will briefly summarize our current understanding of independent regulation of the intrarenal RAS and discuss how inappropriate activation of this system contributes to the development and maintenance of hypertension and renal injury. We will also discuss the impact of antihypertensive agents in preventing the progressive increases in the intrarenal RAS during the development of hypertension and renal injury.

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Interstitial fibroblasts are principal effector cells of organ fibrosis in kidneys, lungs, and liver. While some view fibroblasts in adult tissues as nothing more than primitive mesenchymal cells surviving embryologic development, they differ from mesenchymal cells in their unique expression of fibroblast-specific protein-1 (FSP1). This difference raises questions about their origin. Using bone marrow chimeras and transgenic reporter mice, we show here that interstitial kidney fibroblasts derive from two sources. A small number of FSP1(+), CD34(-) fibroblasts migrate to normal interstitial spaces from bone marrow. More surprisingly, however, FSP1(+) fibroblasts also arise in large numbers by local epithelial-mesenchymal transition (EMT) during renal fibrogenesis. Both populations of fibroblasts express collagen type I and expand by cell division during tissue fibrosis. Our findings suggest that a substantial number of organ fibroblasts appear through a novel reversal in the direction of epithelial cell fate. As a general mechanism, this change in fate highlights the potential plasticity of differentiated cells in adult tissues under pathologic conditions.

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M de Gasparo, K Catt, T Inagami … (2000)

The cardiovascular and other actions of angiotensin II (Ang II) are mediated by AT(1) and AT(2) receptors, which are seven transmembrane glycoproteins with 30% sequence similarity. Most species express a single autosomal AT(1) gene, but two related AT(1A) and AT(1B) receptor genes are expressed in rodents. AT(1) receptors are predominantly coupled to G(q/11), and signal through phospholipases A, C, D, inositol phosphates, calcium channels, and a variety of serine/threonine and tyrosine kinases. Many AT(1)-induced growth responses are mediated by transactivation of growth factor receptors. The receptor binding sites for agonist and nonpeptide antagonist ligands have been defined. The latter compounds are as effective as angiotensin converting enzyme inhibitors in cardiovascular diseases but are better tolerated. The AT(2) receptor is expressed at high density during fetal development. It is much less abundant in adult tissues and is up-regulated in pathological conditions. Its signaling pathways include serine and tyrosine phosphatases, phospholipase A(2), nitric oxide, and cyclic guanosine monophosphate. The AT(2) receptor counteracts several of the growth responses initiated by the AT(1) and growth factor receptors. The AT(4) receptor specifically binds Ang IV (Ang 3-8), and is located in brain and kidney. Its signaling mechanisms are unknown, but it influences local blood flow and is associated with cognitive processes and sensory and motor functions. Although AT(1) receptors mediate most of the known actions of Ang II, the AT(2) receptor contributes to the regulation of blood pressure and renal function. The development of specific nonpeptide receptor antagonists has led to major advances in the physiology, pharmacology, and therapy of the renin-angiotensin system.

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Author and article information

Journal

Journal ID (nlm-ta): Res Rep Urol

Journal ID (iso-abbrev): Res Rep Urol

Journal ID (publisher-id): Research and Reports in Urology

Title: Research and Reports in Urology

Publisher: Dove Medical Press

ISSN (Electronic): 2253-2447

Publication date Collection: 2017

Publication date (Electronic): 12 September 2017

Volume: 9

Pages: 181-186

Affiliations

[1 ]Department of Urology

[2 ]Department of Pathological Anatomy, Hasan Sadikin Hospital, Faculty of Medicine University of Padjadjaran, Bandung, Indonesia

Author notes

Correspondence: Safendra Siregar, Sekretariat Urologi, Hasan Sadikin Hospital, Jalan Pasteur No 38, Bandung, West Java, Indonesia, Tel +62 81 123 2827, Email safendra_sir@ 123456yahoo.co.id

Article

Publisher ID: rru-9-181

DOI: 10.2147/RRU.S141327

PMC ID: 5602470

PubMed ID: 28979891

SO-VID: e4fd2f3a-e117-4ad3-9946-8e0d5f0cf0ed

License:

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