Localization of Calcitonin Receptor mRNA in Rat Kidney: an In Situ Hybridization Study

Ishii, Aiko; Nakamura, Misa; Nakamura, Atsushi; Kimura, Masaaki; Kakudo, Kennichi

doi:10.1267/ahc.37.259

Cited by 7 publications

(5 citation statements)

References 33 publications

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“…The procedure for the ISH analysis was established at our laboratory (Ishii et al, 2004). Briefly, the following primer sequences were used to prepare RNA probes: forward, 5′-CAGGAGTTCTCTGACAATGAGC-3′; and reverse, 5′-AAGCTGTCCTGCATAGCATCTAGG-3′ (NIH accession: NM 053021).…”

Section: Methodsmentioning

confidence: 99%

Molecular Pathological Evaluation of Clusterin in a Rat Model of Unilateral Ureteral Obstruction as a Possible Biomarker of Nephrotoxicity

2007

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In the present study, to determine the validity of considering clusterin as a possible biomarker of nephrotoxicity, the expression and distribution of clusterin in the rat UUO kidney were investigated. Real-time RT-PCR revealed an immediate increase in the clusterin mRNA level in the kidney, within 6 hours after UUO, and also maintenance of the mRNA expression level from day-1 to day-3 was 60-fold higher in the UUO kidney than in the sham kidney. ISH analysis revealed clusterin mRNA signals in the UUO renal tubular epithelium, whereas no signal was observed in the sham kidney. Detection of clusterin-alpha and -beta was conducted using the subtype-specific antibodies, by both of western blotting and immunohistochemistry. Although clusterin-alpha was predominant in the UUO urine, only faint signals were noted at the brush border of the tubular epithelium or intraductal. On the other hand, strong signals of clusterin-beta were detected in the UUO kidney homogenate, and the molecule was localized in the renal tubular epithelium. These results suggest that clusterin was translated in the renal tubular epithelium after de novo expression induced by renal injury. Thus, detection of clusterin mRNA and clusterin-beta in the kidney or clusterin-alpha in the urine may be useful for predicting nephrotoxicity.

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Section: Methodsmentioning

confidence: 99%

Molecular Pathological Evaluation of Clusterin in a Rat Model of Unilateral Ureteral Obstruction as a Possible Biomarker of Nephrotoxicity

2007

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“…These results support the idea that CT-induced CTGF expression is mediated through CT binding sites in renal tubule cells. We have shown expression of CTR mRNA in rat kidney by ISH and demonstrated intensive CTR expression in the proximal and distal tubule (Ishii et al, 2004).…”

Section: Discussionmentioning

confidence: 77%

Calcitonin induces connective tissue growth factor through ERK1/2 signaling in renal tubular cells

et al. 2009

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Calcitonin (CT), a polypeptide hormone, plays important roles in a variety of physiological processes. CT has been used clinically to treat osteoporosis and humoral hypercalcemia of malignancy. In order to clarify the pharmacological effects of CT in the kidney, we identified potential downstream genes induced by CT in the renal cells. Using a cDNA subtraction hybridization method, we identified connective tissue growth factor (CTGF) as a CT-induced gene in the porcine renal cell line, LLC-PK1. Furthermore, we found that CT-mediated induction of the gene was not inhibited by cycloheximide, which suggests that CTGF gene was not induced by an increased synthesis of regulating proteins. Therefore, CTGF is an immediate early gene. We further demonstrated that the regulation of CTGF gene expression by CT involved the ERK1/2 pathway, because PD98059, a MEK1 inhibitor, partially inhibited the mRNA expression of CTGF induced by CT. CT-induced CTGF protein expression was also observed in vivo. Our present findings suggest that CT induces the transcription of CTGF through ERK1/2 phosphorylation. We also identified twelve other genes induced by CT that, like CTGF, were related to wound healing. These results suggest that CT may have an effect on renal differentiation and wound healing in the kidney.

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“…of ISH for CTR mRNA was established in our laboratory [7]. Briefly, the primer sequences of RNA probes were as follows: forward, 5'-ACGACAACTGTTG GCTGAGTAC-3'; and reverse, 5'-CATTCAAGCG GATGAGTCTTGC-3' (accession number: L14617).…”

Section: In Situ Hybridizationmentioning

confidence: 99%

“…CT down-regulates serum levels of calcium by suppressing bone resorption and increasing calcium excretion from the kidney [1][2][3]. Furthermore, both CT and its receptor (CTR) have been identified in a large number of unrelated tissues and cells [4][5][6][7][8], suggesting that CT-CTR might play more roles than just regulating calcium metabolism.…”

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confidence: 99%

“…Recently, we made a detailed report on the distribution of cells that express CTR mRNA in the kidney, using in situ hybridization (ISH) with a newly established specific probe for CTR mRNA [7]. The object of the present study is to localize and quantify CTR mRNA expression in the mammary gland during pregnancy, lactation, and involution, and to determine the effects of CT on DNA synthesis in mammary cells.…”

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confidence: 99%

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Expression of Calcitonin Receptor in Rat Mammary Gland during Lactation

Ishii

Nakamura

et al. 2006

Endocr J

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Abstract. Calcitonin (CT) and calcitonin receptor (CTR) have been reported to play an important role in mammary tissue during pregnancy, lactation, and involution. In the present study, the expression and distribution of CTR mRNA in rat mammary tissue during pregnancy and lactation were investigated. As measured by real-time RT-PCR, CTR mRNA levels were increased only slightly during pregnancy, but increased markedly immediately postpartum and remained elevated through lactation, with the highest levels observed 14 days postpartum. In situ hybridization analysis showed that intense CTR mRNA signals were detected in the whole mammary gland. We performed immunohistochemistry to determine distribution of CTR in the mammary epithelium. CTR has been reported to act as an amylin receptor when heterodimerized with receptor activity modifying protein-1 (RAMP1) or RAMP3. mRNA expression of RAMP1 and RAMP3 in mammary tissue decreased during pregnancy and lactation, and amylin mRNA was undetectable, suggesting that up-regulated CTR in lactating mammary tissues binds CT rather than amylin. In primary cultures of mammary cells isolated from rat dams 14 days postpartum, CT produced a statistically significant decrease in thymidine incorporation. These results suggest that up-regulation of CTR during lactation may contribute to inhibition of mammary epithelial cell proliferation.

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Localization of Calcitonin Receptor mRNA in Rat Kidney: an In Situ Hybridization Study

Cited by 7 publications

References 33 publications

Molecular Pathological Evaluation of Clusterin in a Rat Model of Unilateral Ureteral Obstruction as a Possible Biomarker of Nephrotoxicity

Molecular Pathological Evaluation of Clusterin in a Rat Model of Unilateral Ureteral Obstruction as a Possible Biomarker of Nephrotoxicity

Calcitonin induces connective tissue growth factor through ERK1/2 signaling in renal tubular cells

Expression of Calcitonin Receptor in Rat Mammary Gland during Lactation

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