Molecular distribution and localization of extracellular calcium-sensing receptor (CaSR) and vitamin D receptor (VDR) at three different laying stages in laying hens (Gallus gallus domesticus)

BackgroundTo explore underlying molecular mechanisms in the pathogenesis of symptomatic sporadic primary hyperparathyroidism (PHPT).Materials and methodsForty-one parathyroid adenomas from patients with symptomatic PHPT and ten normal parathyroid glands either from patients with PHPT (n=3) or from euthyroid patients without PHPT during thyroid surgery (n=7) were analyzed for vitamin D receptor (VDR), calcium-sensing receptor (CASR), cyclin D1 (CD1), and parathyroid hormone (PTH) expressions. The protein expressions were assessed semiquantitatively by immunohistochemistry, based on percentage of positive cells and staining intensity, and confirmed by quantitative real-time PCR.ResultsImmunohistochemistry revealed significant reductions in VDR (both nuclear and cytoplasmic) and CASR expressions and significant increases in CD1 and PTH expressions in adenomatous compared with normal parathyroid tissue. Consistent with immunohistochemistry findings, bothVDRandCASRmRNAs were reduced by 0.36- and 0.45-fold change (P<0.001) andCD1andPTHmRNAs were increased by 9.4- and 17.4-fold change respectively (P<0.001) in adenomatous parathyroid tissue.PTHmRNA correlated with plasma PTH (r=0.864;P<0.001), but not with adenoma weight, whileCD1mRNA correlated with adenoma weight (r=0.715;P<0.001). There were no correlations betweenVDRandCASRmRNA levels and serum Ca, plasma intact PTH, or 25-hydroxyvitamin D levels. In addition, there was no relationship between the decreases inVDRandCASRmRNA expressions and the increases inPTHandCD1mRNA expressions.ConclusionsThe expression of both VDR and CASR are reduced in symptomatic PHPT in Asian Indians. In addition,CD1expression was greatly increased and correlated with adenoma weight, implying a potential role for CD1 in adenoma growth and differential clinical expression of PHPT.

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Vitamin D receptor, a tumor suppressor in skin

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2014-0367 ◽

2015 ◽

Vol 93 (5) ◽

pp. 349-354 ◽

Cited By ~ 21

Author(s):

Daniel D. Bikle

Keyword(s):

Vitamin D ◽

Tumor Suppressor ◽

Vitamin D Receptor ◽

Tumor Formation ◽

Calcium Sensing Receptor ◽

Keratinocyte Proliferation ◽

Calcium Sensing ◽

Damage Repair ◽

Proliferation And Differentiation ◽

Active Investigation

Vitamin D and calcium are well-established regulators of keratinocyte proliferation and differentiation. Therefore, it was not a great surprise that deletion of the vitamin D receptor (VDR) should predispose the skin to tumor formation, and that the combination of deleting both the VDR and calcium sensing receptor (CaSR) should be especially pro-oncogenic. In this review I have examined 4 mechanisms that appear to underlie the means by which VDR acts as a tumor suppressor in skin. First, DNA damage repair is curtailed in the absence of the VDR, allowing mutations in DNA to accumulate. Second and third involve the increased activation of the hedgehog and β-catenin pathways in the epidermis in the absence of the VDR, leading to poorly regulated proliferation with reduced differentiation. Finally, VDR deletion leads to a shift in the expression of long noncoding RNAs toward a more oncogenic profile. How these different mechanisms interact and their relative importance in the predisposition of the VDR null epidermis to tumor formation remain under active investigation.

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Vitamin D Receptor and Calcium Sensing Receptor Polymorphisms and the Risk of Colorectal Cancer in European Populations

Cancer Epidemiology Biomarkers & Prevention ◽

10.1158/1055-9965.epi-09-0319 ◽

2009 ◽

Vol 18 (9) ◽

pp. 2485-2491 ◽

Cited By ~ 59

Author(s):

M. Jenab ◽

J. McKay ◽

H. B. Bueno-de-Mesquita ◽

F. J.B. van Duijnhoven ◽

P. Ferrari ◽

...

Keyword(s):

Colorectal Cancer ◽

Vitamin D ◽

Vitamin D Receptor ◽

Calcium Sensing Receptor ◽

Calcium Sensing ◽

European Populations

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Kidney Histopathology of Gallus gallus domesticus Infected by E. coli in Denpasar, Bali

Advances in Tropical Biodiversity and Environmental Sciences ◽

10.24843/atbes.2018.v02.i01.p04 ◽

2018 ◽

Vol 2 (1) ◽

pp. 14

Author(s):

Ni Kadek Prederika Sari Andayani ◽

Iriani Setyawati ◽

Martin Joni

Keyword(s):

Bacterial Infections ◽

Inflammatory Cell ◽

Laying Hens ◽

Gallus Gallus ◽

Gallus Domesticus ◽

Inflammatory Cell Infiltration ◽

Cell Infiltration ◽

Histological Structure ◽

Gallus Gallus Domesticus ◽

E Coli

One of the diseases that attacks poultry especially laying hens (Gallus gallus domesticus) is colibacillosis, a disease caused by Escherichia coli. E. coli is a bacterium that has opportunistic properties, which is normally present in the digestive tract in a controlled amount, but when the condition of the chicken decreases, it can develop into pathogens. Kidneys are organs that are vulnerable to substances that are toxic and are also susceptible to bacterial infections. This study aimed to determine the histological structure of kidneys of laying hens (Gallus gallus domesticus) who died due to the infection of E. coli. The research was conducted at a Pathology Laboratory (BBVet), Denpasar. The hen’s kidneys were processed with the paraffin method and Hematoxylin-Eosin staining. Cell damage that occurs is observed by using the Image Raster application. The data obtained were analyzed with the scoring method. Renal histopathology parameters can be seen in the form of degeneration, necrosis, congestion, and inflammatory cell infiltration. The results obtained cell damages namely 46% of degeneration, 60% of necrosis, 44% of congestion and 76% of inflammatory cell infiltration.

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