Activin A: Autocrine Regulator of Kidney Development and Repair

Maeshima, Akito; Miya, Masaaki; Mishima, Keiichiro; Yamashita, Shinichi; Kojima, Itaru; Nojima, Yoshihisa

doi:10.1507/endocrj.kr-113

Cited by 30 publications

(24 citation statements)

References 71 publications

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“…Although the majority of studies have focused on activin's role in reproduction and development, it is clear that activins also have a role locally in the cellular development and growth of different tissues (Muttukrishna et al 2004, Rodgarkia-Dara et al 2006, Werner & Alzheimer 2006, Maeshima et al 2008. Activins are synthesised as homo-or heterodimers of two highly related disulphide-linked inhibin b subunits (inhibin bA (INBBA) and inhibin bB (INHBB)), which can result in three molecular species activin A, activin AB and activin B (Rodgarkia-Dara et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Inhibin βB expression in murine adipose tissue and its regulation by leptin, insulin and dexamethasone

Hoggard

Cruickshank²,

Moar³

et al. 2009

Journal of Molecular Endocrinology

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Inhibin bB (INHBB; coding for the activin bB subunit) has previously been identified in both human and rodent adipose tissue and using Taqman real-time PCR with specific primers we confirm the expression of INHBB mRNA in rodent adipose tissue. Expression of INHBB in murine epididymal adipose tissue was higher than in any of the other tissues studied and appears to be regulated by changes in energy balance and leptin. It was increased fourfold in the epididymal fat depot of ob/ob mice compared with the same fat depot in lean mice. The i.p. administration of leptin in obese ob/ob mice decreases the expression of INHBB. In human adipose tissue, INHBB is reduced by weight loss. In keeping with this, we demonstrate that INHBB expression in murine adipose tissue is decreased in fasting and increased upon refeeding. We show that INHBB is expressed in both the mature adipocyte and the stromal vascular fraction of adipose tissue. INHBB increases with the differentiation of pre-adipocytes into mature adipocytes in the 3T3-L1 cell line. In differentiated 3T3-L1 adipocytes, where receptors to activin have been previously reported, insulin increases the expression of INHBB, while dexamethasone decreases the expression of INHBB when compared with untreated control cells. Taken together, these results suggest that the regulation of INHBB expression in adipose tissue may play a physiological role in energy balance or the insulin insensitivity associated with obesity.

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Section: Introductionmentioning

confidence: 99%

Inhibin βB expression in murine adipose tissue and its regulation by leptin, insulin and dexamethasone

Hoggard

Cruickshank²,

Moar³

et al. 2009

Journal of Molecular Endocrinology

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“…In an in vitro Wolffi an duct (WD) culture system, activin A was found to negatively regulate ureteric bud (UB) outgrowth from the WD. 12 Activin A also inhibits UB branching, 13,14 and is required for metanephric mesenchyme (MM) differentiation during kidney development. 13 In the kidneys of transgenic mice expressing truncated activin type II receptor, the number of glomeruli was signifi cantly increased when compared to that in wild-type mice.…”

Section: Recapitulation Of the Developmental Paradigm In Kidney Regenmentioning

confidence: 99%

“…12 Activin A also inhibits UB branching, 13,14 and is required for metanephric mesenchyme (MM) differentiation during kidney development. 13 In the kidneys of transgenic mice expressing truncated activin type II receptor, the number of glomeruli was signifi cantly increased when compared to that in wild-type mice. 15 Collectively, it is possible that activin A acts as a negative regulator of renal organogenesis.…”

Section: Recapitulation Of the Developmental Paradigm In Kidney Regenmentioning

confidence: 99%

Label-retaining cells in the kidney: origin of regenerating cells after renal ischemia

Maeshima

2007

Clin Exp Nephrol

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The kidney is capable of regeneration. In response to a variety of insults, renal epithelial tubular cells dedifferentiate into an immature phenotype, proliferate, migrate to the injured area, and redifferentiate into mature polarized epithelial cells. In animal models of acute kidney injury induced by renal ischemia or renal toxins, various growth factors, transcription factors, chemokines, and extracellular matrix components have been demonstrated to be involved in the regeneration process. Recent research has suggested the existence of renal stem/progenitor cells in the kidney and their involvement in renal regeneration. In this review, we will focus on the mechanisms of tubular regeneration after kidney injury, particularly on label-retaining cells actively engaged in this process, and discuss their potential as targets of regenerative therapy for various kidney diseases.

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“…Activin A binds to the type II receptor with the aid of the type Ⅲ receptor, while it can cause the phosphorylation of type I receptor and then form a ternary complex with the phosphorylated type I receptor (7). Smad2 and Smad3 in the cytosol can be phosphorylated by this complex and subsequently transferred into the nucleus, regulating the expression of certain genes (8)(9)(10)(11). Activin A plays an important role in cell proliferation, differentiation, apoptosis and adhesion (12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Activin A expression in esophageal carcinoma and its association with tumor aggressiveness and differentiation

et al. 2015

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Abstract. The aim of the present study was to investigate the expression of activin A in esophageal carcinoma and its association with tumor differentiation and metastasis. A total of 57 esophageal carcinoma patients and 36 controls were included in the current study. The mRNA and protein expression levels of activin A in esophageal tumors or normal esophageal tissues were determined by reverse transcription-quantitative polymerase chain reaction and immunohistochemical analysis. In addition, the association of activin A expression with esophageal carcinoma differentiation, metastasis and recurrence postoperatively was analyzed. The mRNA and protein expression levels of activin A in esophageal carcinoma were significantly higher compared with those in normal esophageal tissues (P<0.05). The expression of activin A was higher in poorly-/moderately-differentiated esophageal tumor tissues compared with that of well-differentiated or control tissues (P<0.05). Furthermore, the expression of activin A in poorly-differentiated esophageal tumor tissues was higher compared with that of moderately-differentiated tissues (P<0.05). A positive correlation was also observed between differentiation degree and activin A expression. The expression of activin A was higher in patients with lymph node metastasis compared with those without metastasis (P<0.05). The cumulative survival rate of patients with a high expression of activin A at 1, 2 and 3 years postoperatively was significantly decreased compared with that of patients with a lower expression of activin A (P<0.05); by contrast, the cumulative recurrence rate was significantly higher in patients with a lower activin A expression (P<0.05).In conclusion, abnormal expression of activin A was detected in esophageal tumor tissues, which was correlated with the tumor differentiation, metastasis, survival and recurrence. In conclusion, activin A may be used as an auxiliary index in the diagnosis and prognosis of clinical esophageal carcinoma.

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Activin A: Autocrine Regulator of Kidney Development and Repair

Cited by 30 publications

References 71 publications

Inhibin βB expression in murine adipose tissue and its regulation by leptin, insulin and dexamethasone

Inhibin βB expression in murine adipose tissue and its regulation by leptin, insulin and dexamethasone

Label-retaining cells in the kidney: origin of regenerating cells after renal ischemia

Activin A expression in esophageal carcinoma and its association with tumor aggressiveness and differentiation

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