Analysis of the SIX2, SIX1 and P300 cistromes in 16-17 week old human fetal kidney cortex

Author(s):  
L O'Brien
2001 ◽  
Vol 86 (10) ◽  
pp. 4627-4629 ◽  
Author(s):  
Hong Zheng ◽  
Genia Radeva ◽  
Jennifer A. McCann ◽  
Geoffrey N. Hendy ◽  
Cynthia G. Goodyer

Pseudohypoparathyroid type 1b patients are characterized by renal resistance to PTH in the absence of Albright’s hereditary osteodystrophy or other endocrine abnormalities. Kindred studies have suggested that the cause of this resistance is a specific decrease in Gαs activity in renal proximal tubules due to paternal imprinting of Gαs. To test this, allelic expression of Gαs was analyzed in human fetal kidney cortex samples by RT-PCR assays. The results showed that, in contrast to the parent-specific expression of exon 1A and XLαs (paternal) or NESP (maternal) mRNAs, Gαs transcripts are biallelically expressed in human kidney cortex. These data implicate abnormal imprinting of alternative regions within the GNAS1 locus as a more likely cause of pseudohypoparathyroid type 1b.


Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1329
Author(s):  
Li Juel Mortensen ◽  
Mette Lorenzen ◽  
Anne Jørgensen ◽  
Jakob Albrethsen ◽  
Niels Jørgensen ◽  
...  

Luteinizing hormone (LH) and human chorionic gonadotropin (hCG) are agonists for the luteinizing hormone receptor (LHCGR) which regulates male reproductive function. LHCGR may be released into body fluids. We wish to determine whether soluble LHCGR is a marker for gonadal function. Cross-sectional, longitudinal, and intervention studies on 195 healthy boys and men and 396 men with infertility, anorchia, or Klinefelter Syndrome (KS) were used to correlate LHCGR measured in serum, seminal fluid, urine, and hepatic/renal artery and vein with gonadal function. LHCGR was determined in fluids from in vitro and in vivo models of human testicular tissue and cell lines, xenograft mouse models, and human fetal kidney and adrenal glands. Western blot showed LHCGR fragments in serum and gonadal tissue of similar size using three different antibodies. The LHCGR-ELISA had no species cross-reactivity or unspecific reaction in mouse serum even after human xenografting. Instead, sLHCGR was released into the media after the culture of a human fetal kidney and adrenal glands. Serum sLHCGR decreased markedly during puberty in healthy boys (p = 0.0001). In healthy men, serum sLHCGR was inversely associated with the Inhibin B/FSH ratio (β −0.004, p = 0.027). In infertile men, seminal fluid sLHCGR was inversely associated with serum FSH (β 0.006, p = 0.009), sperm concentration (β −3.5, p = 0.003) and total sperm count (β −3.2, p = 0.007). The injection of hCG lowered sLHCGR in serum and urine of healthy men (p < 0.01). In conclusion, sLHCGR is released into body-fluids and linked with pubertal development and gonadal function. Circulating sLHCGR in anorchid men suggests that sLHCGR in serum may originate from and possibly exert actions in non-gonadal tissues. (ClinicalTrials: NTC01411527, NCT01304927, NCT03418896).


PLoS ONE ◽  
2009 ◽  
Vol 4 (8) ◽  
pp. e6709 ◽  
Author(s):  
Sally Metsuyanim ◽  
Orit Harari-Steinberg ◽  
Ella Buzhor ◽  
Dorit Omer ◽  
Naomi Pode-Shakked ◽  
...  

2013 ◽  
Vol 46 (1) ◽  
pp. 32 ◽  
Author(s):  
Keisuke Hieda ◽  
Shogo Hayashi ◽  
Ji Hyun Kim ◽  
Gen Murakami ◽  
Baik Hwan Cho ◽  
...  

1986 ◽  
Vol 53 (2) ◽  
pp. 273-279 ◽  
Author(s):  
G. K. Mehrotra ◽  
G. Datta ◽  
K. L. Mukherjee

1995 ◽  
Vol 1 (4) ◽  
pp. 457-466 ◽  
Author(s):  
Patricia M. Kessler ◽  
Sandip P. Vasavada ◽  
Raymond R. Rackley ◽  
Thomas Stackhouse ◽  
Fuh-Mei Duh ◽  
...  

PLoS Biology ◽  
2019 ◽  
Vol 17 (2) ◽  
pp. e3000152 ◽  
Author(s):  
Mazène Hochane ◽  
Patrick R. van den Berg ◽  
Xueying Fan ◽  
Noémie Bérenger-Currias ◽  
Esmée Adegeest ◽  
...  

1999 ◽  
Vol 19 (12) ◽  
pp. 1329-1335 ◽  
Author(s):  
Yung-Hsiao Chiang ◽  
Shinn-Zong Lin ◽  
Cesario V. Borlongan ◽  
Barry J. Hoffer ◽  
Marisela Morales ◽  
...  

The authors, and others, have recently reported that intracerebral administration of glial cell line-derived neurotrophic factor (GDNF) or osteogenic protein-1 protects against ischemia-induced injury in the cerebral cortex of adult rats. Because these trophic factors are highly expressed in the fetal, but not adult, kidney cortex, the possibility that transplantation of fetal kidney tissue could serve as a cellular reservoir for such molecules and protect against ischemic injury in cerebral cortex was examined. Fetal kidneys obtained from rat embryos at gestational day 16, and adult kidney cortex, were dissected and cut into small pieces. Adult male Sprague-Dawley rats were anesthetized with chloral hydrate and placed in a stereotactic apparatus. Kidney tissues were transplanted into three cortical areas adjacent to the right middle cerebral artery (MCA). Thirty minutes after grafting, the right MCA was transiently ligated for 90 minutes. Twenty-four hours after the onset of reperfusion, animals were evaluated behaviorally. It was found that the stroke animals that received adult kidney transplantation developed motor imbalance. However, animals that received fetal kidney grafts showed significant behavioral improvement. Animals were later sacrificed and brains were removed for triphenyltetrazolium chloride staining, Pax-2 immunostaining, and GDNF mRNA expression. It was noted that transplantation of fetal kidney but not adult kidney tissue greatly reduced the volume of infarction in the cerebral cortex. Fetal kidney grafts showed Pax-2 immunoreactivity and GDNF mRNA in the host cerebral cortex. In contrast, GDNF mRNA expression was not found in the adult kidney grafts. Taken together, our data indicate that fetal kidney transplantation reduces ischemia/reperfusion-induced cortical infarction and behavioral deficits in adult rats, and that such tissue grafts could serve as an unique cellular reservoir for trophic factor application to the brain.


Sign in / Sign up

Export Citation Format

Share Document