scholarly journals Mouse Strain Susceptibility to Gonadectomy-Induced Adrenocortical Tumor Formation Correlates with the Expression of GATA-4 and Luteinizing Hormone Receptor

Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 4123-4133 ◽  
Author(s):  
Malgorzata Bielinska ◽  
Helka Parviainen ◽  
Susan B. Porter-Tinge ◽  
Sanne Kiiveri ◽  
Elena Genova ◽  
...  
Keyword(s):  
B Cells ◽  
Inbred Strains ◽  
Tumor Formation ◽  
Luteinizing Hormone Receptor ◽  
Adrenocortical Tumor ◽  
Adrenocortical Cells ◽  
Adrenocortical Tumors ◽  
A Cells ◽  
Inbred Strains Of Mice ◽  
A And B Cells

Abstract Certain inbred strains of mice, including DBA/2J, develop adrenocortical tumors in response to gonadectomy. Spindle-shaped cells with limited steroidogenic capacity, termed A cells, appear in the subcapsular region of the adrenal gland, followed by sex steroid-producing cells known as B cells. These changes result from unopposed gonadotropin production by the pituitary, but the adrenocortical factors involved in tumorigenesis have not been characterized. GATA-4, a transcription factor normally expressed in fetal, but not adult, adrenocortical cells, was found in neoplastic cells that proliferate in the adrenal cortex of gonadectomized DBA/2J mice. GATA-4 mRNA was detected in the adrenal glands of female mice 0.5 months after ovariectomy and reached a maximum by 4 months. Castrated male mice developed adrenocortical tumors more slowly than gonadectomized females, and the onset of GATA-4 expression in the adrenal was delayed. In situ hybridization and immunohistochemistry revealed GATA-4 mRNA and protein in A and B cells, but not in normal adrenocortical cells. mRNA encoding another factor associated with adrenocortical tumorigenesis, LH receptor (LHR), was detected in A and B cells. In addition, transcripts for P450 17α-hydroxylase/C17-C20 lyase, an enzyme essential for the production of sex steroids, and inhibin-α were found in B cells. Unilateral ovarian regeneration, a phenomenon known to occur in gonadectomized mice, was observed in a subset of DBA/2J mice undergoing complete ovariectomy. In these animals, adrenocortical tumor progression was arrested; A cells and GATA-4 expression were evident, but there was no expression of LHR or P450 17α-hydroxylase/C17-C20 lyase. Strain susceptibility to adrenocortical tumorigenesis (DBA/2J ≫ FVB/N) correlated with the expression of GATA-4 and LHR, implicating these factors in the process of adrenocortical neoplasia in response to continuous gonadotropin stimulation.

scholarly journals Frequencies of mitogen-reactive B cells in the mouse. I. Distribution in different lymphoid organs from different inbred strains of mice at different ages

1977 ◽  
Vol 145 (6) ◽  
pp. 1511-1519 ◽  
Author(s):  
J Andersson ◽  
A Coutinho ◽  
F Melchers
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
Thoracic Duct ◽  
Peripheral Blood ◽  
Bone Marrow Cells ◽  
Inbred Strains ◽  
Mesenteric Lymph Nodes ◽  
Inbred Strains Of Mice ◽  
Old Mice

Frequencies of mitogen-reactive B cells have been determined in vitro under culture conditions which allow every growth-inducible B cell to grow and mature into a clone of Ig-secreting PFC. The frequencies of LPS-reactive B cells in the spleen of 6- to 8-wk old mice were between 1 in 3 and 1 in 10 splenic B cells from the following inbred strains of mice: C3H/Tif; BALB/c; BALB/c ν/ν; C57BL/6J; DBA/2J; C57BL/6J x DBA/(2J)F(1); and CBA and A/J. Very similar frequencies are found for lipoprotein-reactive B cells in BALB/c, BALB/c ν/ν, C3H/Tif, and C3H/HeJ mice. No LPS-reactive cells but normal frequencies of lipoprotein-reactive cells were found in C3H/HeJ mice, genetically nonreactive to LPS. SJL mice had significantly lower frequencies of LPS- and of lipoprotein-reactive B cells (1 in approximately 30 B cells). The number of LPS- and of lipoprotein-reactive B cells in spleen was dependent upon the age of the mouse. Newborn spleen contained approximately 10 percent of the number of reactive cells found at 6- to 8-wk of age. From there the frequencies declined again to drop below 5 percent of the maximal number at ages beyond 11 mo. LPS-reactive B cells yielding IgM- and IgG-PFC responses could be found in mesenteric lymph nodes, bone marrow, thymus, thoracic duct, and peripheral blood of 6- to 8-wk old mice. Their frequencies were one in three to five lymph node cells, 1 in 50 to 100 bone marrow cells, one in 10(5) thymus cells, and 1 in 20 to 40 thoracic duct or peripheral blood cells.

scholarly journals AN APPROACH TO THE QUANTITATIVE HISTOCHEMISTRY OF THE A-CELLS IN THE PANCREATIC ISLETS

1966 ◽  
Vol 14 (1) ◽  
pp. 49-52 ◽  
Author(s):  
SVEN E. BROLIN ◽  
ARNE OHLSSON ◽  
ERIK BORGLUND
Keyword(s):  
B Cells ◽  
Islet Cells ◽  
Lactic Dehydrogenase ◽  
Glutamic Oxaloacetic Transaminase ◽  
Malic Dehydrogenase ◽  
Quantitative Histochemistry ◽  
A Cells ◽  
Fresh Frozen ◽  
Darkfield Microscopy ◽  
A And B Cells

Our present knowledge of the quantitative histochemistry of the pancreas is mainly related to the enzymatic properties of the exocrine parenchyma and the B-cells. Appropriate analyses of A-cells require their isolations, which can be accomplished in animals with different islet cells located in separate groups. In fresh frozen sections of the pancreas from ducks groups of A- and B-cells were recognized by darkfield microscopy combined with ordinary microscopic examination after fixation and staining. Each adjacent section was lyophilized and separate samples of acini, A-and B-cells were dissected by free hand. Using quantitative microchemical techniques malic dehydrogenase, lactic dehydrogenase and glutamic-oxaloacetic transaminase activities were measured. The enzymatic distribution found between samples of B-cells and acini was in accordance with earlier findings in mammals, as B-cells showed higher activities except for lactic dehydrogenase. The A-cells differed from the B-cells by lower activities of malic dehydrogenase and glutamic-oxaloacetic transaminase and from the acini by lower activities of lactic dehydrogenase.

Relationship between calbindin-D28K levels in the A and B cells of the rat endocrine pancreas and the secretion of insulin and glucagon: influence of vitamin D3 deficiency and 1,25-dihydroxyvitamin D3

1996 ◽  
Vol 148 (2) ◽  
pp. 223-232 ◽  
Author(s):  
P-M Bourlon ◽  
A Faure-Dussert ◽  
B Billaudel ◽  
B Ch J Sutter ◽  
G Tramu ◽  
...  
Keyword(s):  
Vitamin D ◽  
B Cells ◽  
B Cell ◽  
Vitamin D Deficiency ◽  
Glucagon Secretion ◽  
Calcium Handling ◽  
A Cells ◽  
Calbindin D28k ◽  
Calbindin D ◽  
A And B Cells

Abstract The pancreatic B cell is equipped with specific receptors for 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and contains vitamin D-dependent calcium binding proteins (calbindin-D). Insulin secretion is impaired by vitamin D deficiency and is restored by 1,25-(OH)2D3 (concomitantly with an improved calcium handling within B cells) but the effect of 1,25-(OH)2D3 on the pancreatic B cell via calbindin-D is unclear. Therefore we examined the relationship between calbindin-D28K or calbindin-D9K and the activity of the endocrine pancreas in normal (N), four week vitamin D-deficient (−D) and one week 1,25-(OH)2D3-replete (+D) rats. Calbindin-D9K was not found in the pancreas, neither in the islets nor in the exocrine part, of any of the groups of rats (N, −D, or +D). Surprisingly, total islet calbindin-D28K content was increased by vitamin D deficiency and partly restored by 1,25-(OH)2D3. Calbindin-D28K immunostaining was observed only on A and B cells in the endocrine part of the pancreas, the greatest staining being found in A cells. This difference in staining density was increased by vitamin D deficiency and decreased by 1,25-(OH)2D3 treatment. In vitro, 1,25-(OH)2D3 also produced a negative influence on calbindin-D28K staining in A cells, as demonstrated using pieces of pancreas incubated with the steroid for 2 h. No significant influence on labeling intensity of B cell calbindin-D28K could be shown. Plasma insulin and islet insulin release in response to 10 mm arginine stimulation were decreased in −D rats and enhanced in +D rats towards N values. In contrast, plasma glucagon and the amount of glucagon secretion, stimulated in vitro by 10 mm arginine or by low (1·7 mm) glucose concentration, was increased in −D rats and attenuated by 1,25-(OH)2D3. Thus there appears to be no relationship between the steady state level of B cell calbindin-D28K and the regulation of insulin secretion by 1,25-(OH)2D3 in vitamin D-deficient rats. However there is a correlation between A cell calbindin-D28K and glucagon secretion, which are both negatively regulated by 1,25-(OH)2D3. The predominance of calbindin-D28K in A cells raises the question as to how A and B cells interact and the role of calbindin-D28K in calcium handling. Journal of Endocrinology (1996) 148, 223–232

scholarly journals Functional Relationship Between T15 and J558 Idiotypes in BALB/c Mice

1991 ◽  
Vol 1 (3) ◽  
pp. 213-224 ◽  
Author(s):  
Meenal Vakil ◽  
John F. Kearney
Keyword(s):  
B Cells ◽  
Inbred Strains ◽  
Newborn Mice ◽  
Stage Of Development ◽  
Subsequent Response ◽  
Inbred Strains Of Mice ◽  
Vitro Analysis ◽  
A Minor ◽  
Old Mice

In inbred strains of mice, antiphosphorylcholine (PC) and anti-α1,3 dextran (DEX). antibodies are structurally distinct from each other and have been shown to exhibit noncrossreactive antigen binding and idiotypic specificities. However, the prototype anti-PC and anti-DEX antibodies, TEPC15 and J558, respectively, were shown to be connected via a common autoantiidiotypic monoclonal antibody isolated from newborn BALB/c mice. The capacity of various monoclonal anti-PC and anti-DEX antibodies as well as the antigens PC and DEX to modulate T15 and J558 idiotypes in BALB/c mice was tested by their administration to newborn mice. Anti-PC antibodies of the .T15 idiotype injected into 2-4-day-old mice, at a time when T15 anti-PC precursors develop in BALB/c mice, suppressed the anti- PC response of these mice at 6 weeks of age. Similarly, J558 antibodies injected into 8-12-day-old mice, at a time when J558 precursors normally develop, suppressed the response to DEX. As a further demonstration of this connectivity, the injection of J558 into 4-day-old mice led to a down modulation of T15 idiotype, whereas both T15 and a minor idiotypeexpressing antibody M167 when injected into 8-12-day-old mice caused a reduction in expression of the J558 idiotype. As predicted from in vitro analysis, injection of anti-PC antibodies of the M167 idiotype 2 to 4 days after birth enhanced the subsequent response to PC. However, anti-PC antibodies expressing another minor M603 idiotype did not affect the PC. response. The results parallel thein vitroenhancement of M167 antibodies but not M603 on T15 binding to antiidiotypein vitro. Similarly, anti-DEX antibodies expressing the M104E idiotype had no detectable effects on the capacity to respond to PC or DEX or on the expression of T15 and J558 idiotypes as adults. Exposure of newborn mice to PC led to a dramatic reduction in the response to DEX as adults, whereas exposure to DEX at this stage of development had no effect on response to PC as adults. Collectively, these observations provide evidence for a complex functional connectivity between T15 and J558 idiotype-bearing B cells during ontogeny and extend our previous observations that development of these idiotypes is regulated by idiotype-directed interactions between B cells or their immunoglobulin products.

Effects of Foster Nursing on Alcohol Selection in Inbred Strains of Mice

1972 ◽  
Vol 33 (2) ◽  
pp. 494-503 ◽  
Author(s):  
Setsuo Komura ◽  
Masao Ueda ◽  
Toshikiyo Kobayashi
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice

Duplications and deletions of Vh genes in inbred strains of mice

1988 ◽  
Vol 28 (2) ◽  
pp. 125-135 ◽  
Author(s):  
Adele Tutte ◽  
Roy Riblet
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice ◽  
Vh Genes

scholarly journals THE GENETIC DIVERGENCE OF SUBLINES AS ASSESSED BY HISTOCOMPATIBILITY TESTING

Genetics ◽  
1973 ◽  
Vol 75 (4) ◽  
pp. 671-677
Author(s):  
Willys K Silvers ◽  
David L Gasser
Keyword(s):  
Genetic Divergence ◽  
Inbred Strains ◽  
Skin Grafts ◽  
Inbred Strains Of Mice ◽  
Inbred Rats

ABSTRACT The degree of genetic divergence which has occurred between a number of inbred strains of mice and between two sublines of inbred rats was assessed by determining the fate of inter-subline skin grafts. Sublines which had been separated for 29 and 42 generations possessed no detectable incompatibility, while three combinations of sublines judged to have been maintained apart for from 123 to 129 generations showed slight degrees of histoincompatibility. One pair of sublines which had been separated for 119 generations demonstrated a marked degree of incompatibility, and an F2 test suggested that mutations had occurred at four or five histocompatibility loci.

Sign in / Sign up

Export Citation Format

Share Document