scholarly journals Role of laminin in epithelium formation by F9 aggregates.

1983 ◽  
Vol 97 (1) ◽  
pp. 137-144 ◽  
Author(s):  
A Grover ◽  
G Andrews ◽  
E D Adamson
Keyword(s):  
Basement Membrane ◽  
Morphological Changes ◽  
Embryoid Bodies ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Type I ◽  
Mrna Levels ◽  
Epithelial Layer ◽  
Afp Production

The formation and maturation of the outer epithelial layer is essential for maximal alphafetoprotein (AFP) production during differentiation of F9 embryoid bodies in the presence of 5 X 10(-8) M retinoic acid (Grover et al., 1983. J. Cell Biol. 96:1690-1696). The critical phase is between the third and the fourth day when the components of the extracellular matrix organize into a basement membrane. The role of some of these components in the process of epithelium formation and maturation is analyzed in this paper. The role of laminin was investigated by testing the effect of exogenous laminin and antilaminin in cultures of differentiating F9 aggregates. Tests included growth rates, morphological changes, AFP production, determination of AFP mRNA levels, and fluorescent staining for basement membrane components and for epithelial markers. At concentrations greater than 5 micrograms/ml, exogenous laminin inhibited the production of AFP and prevented AFP gene transcription. On the basis of immunofluorescence tests, exogenous laminin appeared to act by preventing the accumulation of a basement membrane and by disrupting the organization of the outer layer into an epithelium. No such effects were produced by fibronectin or collagens type I or IV. Aggregates cultured in the presence of antilaminin also failed to organize an epithelium and did not produce AFP, whereas those in normal rabbit serum differentiated normally. Therefore, endogenous laminin plays a key role not only as a basement membrane structural component but also in organizing the epithelial layer of endoderm cells and hence (indirectly) in gene expression.

Central administration of alpha-MSH antiserum augments fever in the rabbit

1986 ◽  
Vol 250 (5) ◽  
pp. R803-R806 ◽  
Author(s):  
S. T. Shih ◽  
O. Khorram ◽  
J. M. Lipton ◽  
S. M. McCann
Keyword(s):  
Interleukin 1 ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Central Administration ◽  
Normal Body Temperature ◽  
Melanocyte Stimulating Hormone ◽  
Average Rise ◽  
The Brain ◽  
Antipyretic Action

alpha-Melanocyte-stimulating hormone (alpha-MSH) has a marked antipyretic action when given centrally or peripherally, and the concentration of this peptide within the septal region of the brain increases during fever. To assess the significance of endogenous central alpha-MSH in fever, antiserum was given to rabbits via a cannula implanted in the third cerebral ventricle. Each day for 3 days, the animals received 50 microliters of normal rabbit serum (NRS) or an equal volume of antiserum raised against alpha-MSH. Interleukin 1 (IL 1) was then injected intravenously to determine the effect of central immunoneutralization of alpha-MSH on the febrile response. Immunoneutralization markedly prolonged fever. The average rise in temperature and the area under the fever curve after IL 1 injection were also significantly increased. Antiserum treatment did not alter normal body temperature, and NRS had no effect on IL 1-induced fever. These results indicate that endogenous central alpha-MSH contributes to physiological limitation of fever and that the role of this peptide in temperature regulation is relevant to the febrile state but not to normothermia.

scholarly journals Role of Osteoglycin in the Linkage between Muscle and Bone

2012 ◽  
Vol 287 (15) ◽  
pp. 11616-11628 ◽  
Author(s):  
Ken-ichiro Tanaka ◽  
Erika Matsumoto ◽  
Yoshiko Higashimaki ◽  
Takenobu Katagiri ◽  
Toshitsugu Sugimoto ◽  
...  
Keyword(s):  
Transcriptional Activity ◽  
Type I Collagen ◽  
C2c12 Cells ◽  
Type I ◽  
Mrna Levels ◽  
Humoral Factors ◽  
Anabolic Activity ◽  
Morphogenetic Protein ◽  
Muscle Tissues

The interaction between muscle tissues and bone metabolism is incompletely understood. We hypothesized that there might be some humoral factors that are produced in muscle tissues and exhibit bone anabolic activity. We, therefore, performed comparative DNA microarray analysis between mouse myoblastic C2C12 cells transfected with either stable empty vector or ALK2 (R206H), the mutation that constitutively activates the bone morphogenetic protein (BMP) receptor, to search for muscle-derived bone anabolic factors. Twenty-five genes whose expression was decreased to <1/4, were identified; these included osteoglycin (OGN). Stable overexpression of OGN significantly decreased the levels of Runx2 and Osterix mRNA compared with those in cells transfected with vector alone in MC3T3-E1 cells. On the other hand, it significantly enhanced the levels of alkaline phosphatase (ALP), type I collagen (Col1), and osteocalcin (OCN) mRNA as well as β-catenin and mineralization. A reduction in endogenous OGN level showed the opposite effects to those of OGN overexpression in MC3T3-E1 and mouse calvarial osteoblastic cells. Transient OGN overexpression significantly suppressed the levels of Runx2, Osterix, ALP, Col1, and OCN mRNA induced by BMP-2 in C2C12 cells. The conditioned medium from OGN-overexpressed and OGN-suppressed myoblastic cells enhanced and decreased, respectively, the levels of ALP, Col1, and β-catenin in MC3T3-E1 cells. Moreover, OGN increased Smad3/4-responsive transcriptional activity as well as Col1 mRNA levels independently of endogenous TGF-β in these cells. In conclusion, this study suggests that OGN may be a crucial humoral bone anabolic factor that is produced by muscle tissues.

scholarly journals Role of type I interferon in the bacillus Calmette-Guérin-induced expression of CXCL10 from human monocytes

2004 ◽  
Vol 13 (5-6) ◽  
pp. 343-348 ◽  
Author(s):  
Patricia Méndez Samperio ◽  
Artemisa Trejo ◽  
Elena Miranda
Keyword(s):  
Polymerase Chain Reaction ◽  
Polymerase Chain Reaction Method ◽  
Type I ◽  
Mrna Levels ◽  
Human Monocytes ◽  
Bacillus Calmette Guerin ◽  
Chain Reaction ◽  
Reaction Method ◽  
Polymerase Chain

BACKGROUND: The proinflammatory chemokine CXCL10, in addition to its chemotactic properties, is also involved in the stimulation of natural killer and T-cell migration inMycobacterium tuberculosisinfection. In this study, our experiments were designed to determine the role of interferon (IFN)-αβ in the production of CXCL10 by human monocytes infected withMycobacterium bovisbacillus Calmette-Guérin (BCG).Methods: The concentrations of CXCL10 in culture supernatants of monocytes infected withM. bovisBCG were determined by enzyme-linked immunosorbent assay. CXCL10 mRNA levels were determined by the reverse transcription-polymerase chain reaction method.Results: We have shown the induction of CXCL10 following infection withM. bovisBCG in a dose-dependent and time-dependent manner. Importantly, the secretion of CXCL10 in response toM. boviswas increased by IFN-α. These results were further confirmed by the fact that the addition of an anti-IFN-αβ neutralizing antibody completely reversed the stimulatory effect, whereas an isotype-matched control antibody had no significant effect on CXCL10 secretion. It is important to note that no significant effect of type I IFN on CXCL8 production inM. bovis-infected monocytes was observed. This was consistent with the finding by the reverse transcription-polymerase chain reaction method that treatment with anti-IFN-α/β antibodies potentially inhibited CXCL10 mRNA levels, whereas no significant effect was observed on CXCL8 mRNA. Moreover, in THP-1 monocytes and THP-1 macrophages, the addition of exogenous IFN-α stimulated CXCL10 secretion.Conclusions: Collectively, these results indicate that the type I IFN may play an important role to modulate the expression of CXCL10 inM. bovisBCG infection. Studies onM. bovis-induced chemokine secretion could provide important insight into the regulation of the immune response against tuberculosis.

Inactivation of White Spot Syndrome Virus (WSSV) by normal rabbit serum: Implications for the role of the envelope protein VP28 in WSSV infection of shrimp

2006 ◽  
Vol 118 (1-2) ◽  
pp. 55-61 ◽  
Author(s):  
Javier Robalino ◽  
Caroline Payne ◽  
Pamela Parnell ◽  
Eleanor Shepard ◽  
Adrian C. Grimes ◽  
...  
Keyword(s):  
Envelope Protein ◽  
White Spot Syndrome Virus ◽  
White Spot ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
White Spot Syndrome

scholarly journals Mesangiocapillary glomerulonephritis.

1992 ◽  
Vol 2 (10) ◽  
pp. S159
Author(s):  
G D'Amico ◽  
F Ferrario
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Inflammatory Cells ◽  
Type I ◽  
Mesangiocapillary Glomerulonephritis ◽  
Dense Deposits ◽  
Table Analysis ◽  
System Activation ◽  
Morphological Variants

The clinical and histological features of idiopathic mesangiocapillary glomerulonephritis (MCGN) have been reviewed, with a survey of the most recent literature, including the retrospective analysis of the data of the Italian Study Group of Renal Immunopathology on 368 patients. In both major types of MCGN, six morphological variants have been characterized (classical MCGN, nodular MCGN, exudative MCGN, focal segmental MCGN, MCGN with massive deposits, and crescentic MCGN) that have different etiologic, pathogenetic, or clinical outcome correlates. Actuarial renal survival 10 yr after renal biopsy has been calculated with life-table analysis to be 60 to 65% in type I MCGN, without significant differences between treated and untreated patients; none of the therapeutic regimens tested up to now for this disease have been independently demonstrated to be efficacious. As for the pathogenesis, the interrelationships between the three mechanisms that contribute to the development of the morphological features of the disease (accumulation of electron-dense deposits on the subendothelial side of the glomerular basement membrane or within the glomerular basement membrane; mesangial proliferation and peripheral interposition; and inflow of inflammatory cells, mainly monocytes) have been discussed, and the role of hypocomplementemia and circulating nephritic factors (NFa and NFt) has been analyzed. Available evidence suggests that MCGN is an immunocomplex-mediated disease, the deposition of immune deposits being the initiating phenomenon, whereas the morphologic changes and complement system activation are secondary events.

Antiserum against tumor necrosis factor enhances lipopolysaccharide fever in rats

1990 ◽  
Vol 258 (2) ◽  
pp. R332-R337 ◽  
Author(s):  
N. C. Long ◽  
S. L. Kunkel ◽  
A. J. Vander ◽  
M. J. Kluger
Keyword(s):  
Tumor Necrosis Factor ◽  
Intramuscular Injection ◽  
Tumor Necrosis ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Control Serum ◽  
Necrosis Factor

The role of tumor necrosis factor (TNF, cachectin), a putative endogenous pyrogen, was investigated by comparing fever and plasma TNF levels after the intraperitoneal and intramuscular injection of 10 micrograms/kg lipopolysaccharide (LPS) into male Sprague-Dawley rats and by neutralization of endogenous TNF using TNF antiserum. An intraperitoneal injection of LPS caused a biphasic fever that lasted approximately 6.5 h. TNF levels in these rats peaked at 657 +/- 222 U/ml at 1 h then declined to virtually undetectable levels by the fourth hour. The intramuscularly injected animals showed a lower monophasic fever and low sustained TNF levels (40 +/- 10 U/ml at 1 h, 18 +/- 11 U/ml at 4 h). In a second study, an antiserum that had been shown to neutralize rat TNF was injected intraperitoneally 2 h before the intramuscular injection of 10 micrograms/kg LPS. Control rats were injected with normal rabbit serum before LPS. During the second hour after the injection of LPS, the animals that received the antiserum developed fevers that tended to be lower than those seen in the rats that were injected with control serum (0.33 +/- 0.06 vs. 0.58 +/- 0.1), although this difference was not significant. However, during the third through eighth hours after LPS, the antiserum-injected rats had mean body temperatures that were significantly higher than those of the control rats (1.62 +/- 0.11 vs. 1.07 +/- 0.09; P = 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)

The role of somatostatin and/or dopamine in basal and TRH-stimulated TSH release in food-restricted rats

1991 ◽  
Vol 125 (2) ◽  
pp. 186-191 ◽  
Author(s):  
Felipe Rodriguez ◽  
Trinidad Jolin
Keyword(s):  
Rabbit Serum ◽  
Dopamine Antagonists ◽  
Normal Rabbit Serum ◽  
Restricted Feeding ◽  
Gh Secretion ◽  
Endogenous Dopamine ◽  
Tsh Secretion ◽  
Anterior Pituitary Function ◽  
Plasma Gh

Abstract. The present study was carried out to examine the role of endogenous dopamine and somatostatin in the mechanisms involved in the restricted feeding-induced inhibition of TSH secretion in rats. GH secretion was examined in parallel. Restricted feeding by 50% or 75% was associated with a decrease in the pituitary and circulating levels of TSH and GH in both untreated and TRH-treated groups (p<0.001), the changes being proportional to the feeding level. Intravenous injections of the dopamine antagonists, domperidone or haloperidol, failed to affect the magnitude of the differences in plasma TSH and GH levels among control and food-restricted groups, indicating that dopaminergic mechanisms had little effect on the regulation of TSH and GH secretion during restricted feeding in rats. Cerebroventricular injection of somatostatin anti-serum resulted in a marked increase in plasma TSH and GH levels in all the experimental groups (p<0.001). The increase in plasma GH and TSH induced by somatostatin anti-serum was greater in rats fed a 25% diet than in either controls or rats fed 50% of the diet; the values for the latter two groups were also different (p<0.001). The decreased TSH and GH values in somatostatin anti-serum-treated food restricted rats as compared with those in control animals on somatostatin anti-serum or normal rabbit serum can probably be attributed to the decreased available pituitary TSH and GH pools. The data indicate that long-term restricted feeding affects anterior pituitary function in rats, presumably reflecting alterations in the secretion of an inhibiting hormone, somatostatin.

scholarly journals Deletion of Alox15 improves kidney dysfunction and inhibits fibrosis by increased PGD2 in the kidney

2021 ◽  
Vol 25 (5) ◽  
pp. 445-455
Author(s):  
Naohiro Takahashi ◽  
Hiroaki Kikuchi ◽  
Ayaka Usui ◽  
Taisuke Furusho ◽  
Takuya Fujimaru ◽  
...  
Keyword(s):  
Type I Collagen ◽  
Interstitial Fibrosis ◽  
Mrna Level ◽  
Type I ◽  
Renal Tubules ◽  
Mrna Levels ◽  
Metabolizing Enzymes ◽  
Protein Levels ◽  
Lipid Metabolizing Enzymes

Abstract Background Lipid-metabolizing enzymes and their metabolites affect inflammation and fibrosis, but their roles in chronic kidney disease (CKD) have not been completely understood. Methods To clarify their role in CKD, we measured the mRNA levels of major lipid-metabolizing enzymes in 5/6 nephrectomized (Nx) kidneys of C57BL/6 J mice. Mediator lipidomics was performed to reveal lipid profiles of CKD kidneys. Results In 5/6 Nx kidneys, both mRNA and protein levels of Alox15 were higher when compared with those in sham kidneys. With respect to in situ hybridization, the mRNA level of Alox15 was higher in renal tubules of 5/6 Nx kidneys. To examine the role of Alox15 in CKD pathogenesis, we performed 5/6 Nx on Alox15−/− mice. Alox15−/− CKD mice exhibited better renal functions than wild-type mice. Interstitial fibrosis was also inhibited in Alox15−/− CKD mice. Mediator lipidomics revealed that Alox15−/− CKD mouse kidneys had significantly higher levels of PGD2 than the control. To investigate the effects of PGD2 on renal fibrosis, we administered PGD2 to TGF-β1-stimulated NRK-52E cells and HK-2 cells, which lead to a dose-dependent suppression of type I collagen and αSMA in both cell lines. Conclusion Increased PGD2 in Alox15−/− CKD mouse kidneys could inhibit fibrosis, thereby resulting in CKD improvement. Thus, Alox15 inhibition and PGD2 administration may be novel therapeutic targets for CKD.

scholarly journals Human Prostate Epithelial Cells Activate the AIM2 Inflammasome upon Cellular Senescence: Role of POP3 Protein in Aging-Related Prostatic Inflammation

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 366
Author(s):  
Ravichandran Panchanathan ◽  
Vaikundamoorthy Ramalingam ◽  
Hongzhu Liu ◽  
Divaker Choubey
Keyword(s):  
Epithelial Cells ◽  
Cell Line ◽  
Type I ◽  
Mrna Levels ◽  
Normal Prostate ◽  
Prostate Hyperplasia ◽  
Prostate Epithelial Cells ◽  
Prostatic Inflammation ◽  
Benign Prostate

Increased levels of type I (T1) interferon (IFN)-inducible POP3 protein in myeloid cells inhibit activation of the AIM2 inflammasome and production of IL-1β and IL-18 proinflammatory cytokines. The AIM2 mRNA levels were significantly higher in benign prostate hyperplasia (BPH) than the normal prostate. Further, human normal prostate epithelial cells (PrECs), upon becoming senescent, activated an inflammasome. Because in aging related BPH senescent PrECs accumulate, we investigated the role of POP3 and AIM2 proteins in pre-senescent and senescent PrECs. Here we report that the basal levels of the POP3 mRNA and protein were lower in senescent (versus young or old) PrECs that exhibited activation of the T1 IFN response. Further, treatment of PrECs and a BPH cell line (BPH-1) that expresses the androgen receptor (AR) with the male sex hormone dihydrotestosterone (DHT) increased the basal levels of POP3 mRNA and protein, but not AIM2, and inhibited activation of the AIM2 inflammasome. Of interest, a stable knockdown of POP3 protein expression in the BPH-1 cell line increased cytosolic DNA-induced activation of AIM2 inflammasome. These observations suggest a potential role of POP3 protein in aging-related prostatic inflammation.

scholarly journals Regulation of the differentiation and behaviour of extra-embryonic endodermal cells by basement membranes

2001 ◽  
Vol 114 (5) ◽  
pp. 931-939 ◽  
Author(s):  
P. Murray ◽  
D. Edgar
Keyword(s):  
Stem Cells ◽  
Basement Membrane ◽  
Embryonic Stem ◽  
Basement Membranes ◽  
Embryoid Bodies ◽  
Endodermal Differentiation ◽  
And Migration ◽  
The Individual ◽  
Endodermal Cells

Both the extracellular matrix and parathyroid hormone-related peptide (PTHrP) have been implicated in the differentiation and migration of extra-embryonic endodermal cells in the pre-implantation mammalian blastocyst. In order to define the individual roles and interactions between these factors in endodermal differentiation, we have used embryoid bodies derived from Lamc1(-/-) embryonic stem cells that lack basement membranes. The results show that in the absence of basement membranes, increased numbers of both visceral and parietal endodermal cells differentiate, but they fail to form organised epithelia. Furthermore, although parietal endodermal cells only migrate away from control embryoid bodies in the presence of PTHrP, they readily migrate from Lamc1(-/-) embryoid bodies in the absence of PTHrP, and this migration is unaffected by PTHrP. Thus, the basement membrane between epiblast and extra-embryonic endoderm is required for the proper organisation of visceral and parietal endodermal cells and also restricts their differentiation to maintain the population of primitive endodermal stem cells. Moreover, this basement membrane inhibits migration of parietal endodermal cells, the role of PTHrP being to stimulate delamination of parietal endodermal cells from the basement membrane rather than promoting migration per se.

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