Expression of mitogen-activated protein kinase family in rat renal development

Omori, Sayu; Hida, Mariko; Ishikura, Kenji; Kuramochi, Shigeru; Awazu, Midori

doi:10.1046/j.1523-1755.2000.00137.x

Cited by 52 publications

(55 citation statements)

References 18 publications

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“…We ourselves have previously shown the speci®city of this antibody under the same conditions by showing colocalisation of TNFa, TRAF-2 and total NF-kB staining with the active NF-kB staining and showing clear nuclear localisation of the active NF-kB (van Den Brink et al, 2000). Phosphospeci®c antibodies are also increasingly being used in immunohistochemistry in formalin ®xed, para n embedded tissue, especially pJNK and pp38 MAPK (Omori et al, 2000;Pirvola et al, 2000). Speci®city is usually con®rmed by showing results from immunoblot experiments.…”

Section: Discussionmentioning

confidence: 99%

NF-kappaB, p38 MAPK and JNK are highly expressed and active in the stroma of human colonic adenomatous polyps

et al. 2001

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The factors that govern the progression from colonic adenomatous polyp to colon cancer are poorly understood. The observation that NSAIDs act as chemopreventative agents and reduce the size of colonic polyps suggests the involvement of in¯ammatory signalling, but in¯ammatory signalling in colonic polyps has not been studied. We investigated the expression of the active forms of NF-kB, JNK and p38 MAPK using immunohistochemistry with activation speci®c antibodies in human colonic adenomas. We show that active NF-kB is seen in stromal macrophages that also express COX-2 and TNF-a, active JNK is seen in stromal and intraepithelial T-lymphocytes and periendothelial cells of new blood vessels, and active p38 MAPK is most highly expressed in macrophages and other stromal cells. These results demonstrate the presence of active in¯ammatory signal transduction in colonic polyps and that these are predominantly in the stroma. In the case of NF-kB this coincides with the cellular localisation of COX-2. These results support evidence that NSAIDs may act through e ects on stromal cells rather than epithelial cells. Oncogene (2001) 20, 819 ± 827.

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Section: Discussionmentioning

confidence: 99%

NF-kappaB, p38 MAPK and JNK are highly expressed and active in the stroma of human colonic adenomatous polyps

et al. 2001

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“…Immunoblot analyses of kidney homogenates, as well as immunohistochemical studies, have indicated that ERK and p38 MAPKs are predominantly expressed in the developing kidney, the highest levels being observed in the embryo (10). The role of JNK MAPK in embryogenesis has been investigated, and it has been shown that the loss of the MKK4 gene, a JNK activator, results in embryonic death (26).…”

Section: Evidence For the Role Of Mapk In Kidney Developmentmentioning

confidence: 99%

“…AII stimulates mesangial cells to produce various ECM components in cell culture studies (6), and also promotes cell proliferation and differentiation (7). It has also been shown that human fetal mesangial cells express α-SM-actin (8,9) and that large-scale cell proliferation occurs during kidney development (10). Up-regulated α-SM-actin synthesis by mesangial cells is frequently associated with increased cell proliferation and ECM production (11).…”

Section: Introductionmentioning

confidence: 99%

Roles of mitogen-activated protein kinases and angiotensin II in renal development

Balbi

Francescato

Marin

et al. 2009

Braz J Med Biol Res

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Experimental and clinical evidence suggests that angiotensin II (AII) participates in renal development. Renal AII content is several-fold higher in newborn rats and mice than in adult animals. AII receptors are also expressed in higher amounts in the kidneys of newborn rats. The kidneys of fetuses whose mother received a type 1 AII receptor (AT 1 ) antagonist during gestation present several morphological alterations. Mutations in genes that encode components of the renin-angiotensin system are associated with autosomal recessive renal tubular dysgenesis. Morphological changes were detected in the kidneys of 3-weekold angiotensin-deficient mice. Mitogen-activated protein kinases (MAPKs) are important mediators that transduce extracellular stimuli to intracellular responses. The MAPK family comprises three major subgroups, namely extracellular signal-regulated protein kinase (ERK), c-jun N-terminal kinases (JNK), and p38 MAPK (p38). Important events in renal growth during nephrogenesis such as cellular proliferation and differentiation accompanied by apoptosis on a large scale can be mediated by MAPK pathways. A decrease in glomerulus number was observed in embryos cultured for 48 and 120 h with ERK or p38 inhibitors. Many effects of AII are mediated by MAPK pathways. Treatment with losartan during lactation provoked changes in renal function and structure associated with alterations in AT 1 and type 2 AII (AT 2 ) receptors and p-JNK and p-p38 expression in the kidney. Several studies have shown that AII and MAPKs play an important role in renal development. However, the relationship between the effects of AII and MAPK activation on renal development is still unclear.

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“…p38 MAPK and JNK signaling is evident during kidney development in the rat (8). This appears to be important in kidney development since the addition of a p38 inhibitor to cultured metanephroi impaired cell proliferation and nephrogenesis (9).…”

Section: Sapk In Renal Physiologymentioning

confidence: 99%

The role of stress-activated protein kinase signaling in renal pathophysiology

Liu

Nikolic-Paterson

2008

Braz J Med Biol Res

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Two major stress-activated protein kinases are the p38 mitogen-activated protein kinase (MAPK) and the c-Jun amino terminal kinase (JNK). p38 and JNK are widely expressed in different cell types in various tissues and can be activated by a diverse range of stimuli. Signaling through p38 and JNK is critical for embryonic development. In adult kidney, p38 and JNK signaling is evident in a restricted pattern suggesting a normal physiological role. Marked activation of both p38 and JNK pathways occurs in human renal disease, including glomerulonephritis, diabetic nephropathy and acute renal failure. Administration of small molecule inhibitors of p38 and JNK has been shown to provide protection from renal injury in different types of experimental kidney disease through inhibition of renal inflammation, fibrosis, and apoptosis. In particular, a role for JNK signaling has been identified in macrophage activation resulting in up-regulation of pro-inflammatory mediators and the induction of renal injury. The ability to provide renal protection by blocking either p38 or JNK indicates a lack of redundancy for these two signaling pathways despite their activation by common stimuli. Therefore, the stress-activated protein kinases, p38 and JNK, are promising candidates for therapeutic intervention in human renal diseases.

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Expression of mitogen-activated protein kinase family in rat renal development

Abstract: ERK, p38, and MKP-1 are strongly expressed in developing kidney, and JNK is detected predominantly in adult kidney. Both the temporal and spatial expression of ERK coincides with the maturation of the kidney.

Cited by 52 publications

References 18 publications

NF-kappaB, p38 MAPK and JNK are highly expressed and active in the stroma of human colonic adenomatous polyps

NF-kappaB, p38 MAPK and JNK are highly expressed and active in the stroma of human colonic adenomatous polyps

Roles of mitogen-activated protein kinases and angiotensin II in renal development

The role of stress-activated protein kinase signaling in renal pathophysiology

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