Alterations in somite patterning of Myf-5-deficient mice: a possible role for FGF-4 and FGF-6

Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 141-150 ◽  
Author(s):  
S. Grass ◽  
H.H. Arnold ◽  
T. Braun
Keyword(s):  
Potential Role ◽  
Perinatal Death ◽  
Close Contact ◽  
Substantial Reduction ◽  
Tgf Beta ◽  
Targeted Mutation ◽  
Myogenic Factor ◽  
Beta 2 ◽  
Deficient Mice

Mice carrying a targeted mutation in the gene for the myogenic factor Myf-5 fail to form major parts of the ribs, which leads to an unstable thorax and perinatal death. Here, we report that somites of Myf-5-deficient mice lack the expression of FGF-4 and FGF-6 while TGF beta-2 is expressed normally. Early sclerotomal markers, such as Pax-1 reveal no substantial reduction of sclerotome size. At E11.5 the condensing mesenchyme of the rib anlagen is considerably reduced in size in Myf-5 mutant mice. This may be caused by the lack of Myf-5-positive, FGF-expressing cells which normally are in close contact with the lateral sclerotome generating the rib progenitors. The potential role of FGFs and TGF beta on sclerotome formation is demonstrated in micromass cultures of early somites. Combinations of FGF-4 or FGF-6 with TGF beta-2 potentiate chondrogenesis suggesting that these growth factors emanating from early myotomal and dermomyotomal cells may have instructive or permissive effects on differentiation or outgrowth of sclerotomal cells.

scholarly journals Impaired thrombin generation in Reelin-deficient mice: a potential role of plasma Reelin in hemostasis

2014 ◽  
Vol 12 (12) ◽  
pp. 2054-2064 ◽  
Author(s):  
W.-L. Tseng ◽  
T.-H. Chen ◽  
C.-C. Huang ◽  
Y.-H. Huang ◽  
C.-F. Yeh ◽  
...  
Keyword(s):  
Thrombin Generation ◽  
Potential Role ◽  
Deficient Mice

scholarly journals Potential Role of the Chemokine Macrophage Inflammatory Protein 1α in Human and Experimental Schistosomiasis

2005 ◽  
Vol 73 (4) ◽  
pp. 2515-2523 ◽  
Author(s):  
Adriano L. S. Souza ◽  
Ester Roffê ◽  
Vanessa Pinho ◽  
Danielle G. Souza ◽  
Adriana F. Silva ◽  
...  
Keyword(s):  
Potential Role ◽  
Severe Disease ◽  
Experimental Studies ◽  
Interleukin 4 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein ◽  
Deficient Mice

ABSTRACT In human schistosomiasis, the concentrations of the chemokine macrophage inflammatory protein 1α (MIP-1α/CCL3) is greater in the plasma of patients with clinical hepatosplenic disease. The objective of the present study was to confirm the ability of CCL3 to detect severe disease in patients classified by ultrasonography (US) and to evaluate the potential role of CCL3 in Schistosoma mansoni-infected mice. CCL3 was measured by enzyme-linked immunosorbent assay in the plasma of S. mansoni-infected patients. CCL3-deficient mice were infected with 25 cercariae, and various inflammatory and infectious indices were evaluated. The concentration of CCL3 was higher in the plasma of S. mansoni-infected than noninfected patients. Moreover, CCL3 was greater in those with US-defined hepatosplenic than with the intestinal form of the disease. In CCL3-deficient mice, the size of the granuloma and the liver eosinophil peroxidase activity and collagen content were diminished compared to wild-type mice. In CCL3-deficient mice, the worm burden after 14 weeks of infection, but not after 9 weeks, was consistently smaller. The in vitro response of mesenteric lymph node cells to antigen stimulation was characterized by lower levels of interleukin-4 (IL-4) and IL-10. CCL3 is a marker of disease severity in infected humans, and experimental studies in mice suggest that CCL3 may be a causative factor in the development of severe schistosomiasis.

Mesoderm induction in amphibians: the role of TGF-beta 2-like factors

Science ◽  
1988 ◽  
Vol 239 (4841) ◽  
pp. 783-785 ◽  
Author(s):  
F Rosa ◽  
A. Roberts ◽  
D Danielpour ◽  
L. Dart ◽  
M. Sporn ◽  
...  
Keyword(s):  
Mesoderm Induction ◽  
Tgf Beta ◽  
Beta 2

scholarly journals Cell-autonomous role of TGFβ and IL-2 receptors in CD4+ and CD8+ inducible regulatory T-cell generation during GVHD

Blood ◽  
2012 ◽  
Vol 119 (23) ◽  
pp. 5575-5583 ◽  
Author(s):  
Norifumi Sawamukai ◽  
Atsushi Satake ◽  
Amanda M. Schmidt ◽  
Ian T. Lamborn ◽  
Priti Ojha ◽  
...  
Keyword(s):  
T Cells ◽  
Potential Role ◽  
Acute Gvhd ◽  
De Novo ◽  
Receptor Expression ◽  
Tgfβ Receptor ◽  
Bona Fide ◽  
Deficient Mice ◽  
Transplantation Recipient

Abstract FoxP3+ regulatory T cells (Tregs) suppress GVHD while preserving graft-versus-tumor effects, making them an attractive target for GVHD therapy. The donor-derived Treg pool can potentially be derived from the expansion of preexisting natural Tregs (nTregs) or from de novo generation of inducible Tregs (iTregs) from donor Tconvs in the transplantation recipient. Using an MHC-mismatched model of acute GVHD, in the present study we found that the Treg pool was comprised equally of donor-derived nTregs and iTregs. Experiments using various combinations of T cells from wild-type and FoxP3-deficient mice suggested that both preexisting donor nTregs and the generation of iTregs in the recipient mice contribute to protection against GVHD. Surprisingly, CD8+FoxP3+ T cells represented approximately 70% of the iTreg pool. These CD8+FoxP3+ T cells shared phenotypic markers with their CD4+ counterparts and displayed suppressive activity, suggesting that they were bona fide iTregs. Both CD4+ and CD8+ Tregs appeared to be protective against GVHD-induced lethality and required IL-2 and TGFβ receptor expression for their generation. These data illustrate the complex makeup of the donor-derived FoxP3+ Treg pool in allogeneic recipients and their potential role in protection against GVHD.

scholarly journals Potential role of ATM in hepatocyte endocytosis of ApoE-deficient, ApoB48-containing lipoprotein in ApoE-deficient mice

2013 ◽  
Vol 33 (2) ◽  
pp. 462-468 ◽  
Author(s):  
JIANHUA WU ◽  
YANHONG XIAO ◽  
JUANG LIU ◽  
HONG YANG ◽  
XIAOMIN DONG ◽  
...  
Keyword(s):  
Potential Role ◽  
Deficient Mice

Role of TGF beta s and BMPs as signals controlling the position of the digits and the areas of interdigital cell death in the developing chick limb autopod

Development ◽  
1996 ◽  
Vol 122 (8) ◽  
pp. 2349-2357 ◽  
Author(s):  
Y. Ganan ◽  
D. Macias ◽  
M. Duterque-Coquillaud ◽  
M.A. Ros ◽  
J.M. Hurle
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Ectopic Expression ◽  
Local Administration ◽  
Tgf Beta ◽  
Signal Characteristic ◽  
Beta 2 ◽  
Interdigital Cell Death ◽  
Ectopic Area

The establishment of the digital rays and the interdigital spaces in the developing limb autopod is accompanied by the occurrence of corresponding domains of expression of TGF beta s and BMPs. This study analyzes whether these coincident events are functionally correlated. The experiments consisted of local administration of TGF beta-1, TGF beta-2 or BMP-4 by means of heparin or Affi-gel blue beads to the chick limb autopod in the stages preceding the onset of interdigital cell death. When beads bearing either TGF beta-1 or −2 were implanted in the interdigits, the mesodermal cells were diverted from the death program forming ectopic cartilages or extra digits in a dose- and stage-dependent fashion. This change in the interdigital phenotype was preceded by a precocious ectopic expression of ck-erg gene around the bead accompanied by down-regulation of bmp-4, msx-1 and msx-2 gene expression. When BMP-beads were implanted in the interdigital spaces, programmed cell death and the freeing of the digits were both accelerated. Implantation of beads bearing BMP-4 at the tip of the growing digits was followed by digit bifurcation, accompanied by the formation of an ectopic area of cell death resembling an extra interdigit, both morphologically and molecularly. The death-inducing effect of the BMP beads and the chondrogenic-inducing effect of the TGF beta beads were antagonized by the implantation of an additional bead preabsorbed with FGF-2, which constitutes a signal characteristic of the progress zone. It is concluded that the spatial distribution of digital rays and interdigital spaces might be controlled by a patterned distribution of TGF beta s and BMPs in the mesoderm subjacent to the progress zone.

scholarly journals Monosodium iodoacetate-induced inflammation and joint pain are reduced in TRPA1 deficient mice – potential role of TRPA1 in osteoarthritis

2015 ◽  
Vol 23 (11) ◽  
pp. 2017-2026 ◽  
Author(s):  
L.J. Moilanen ◽  
M. Hämäläinen ◽  
E. Nummenmaa ◽  
P. Ilmarinen ◽  
K. Vuolteenaho ◽  
...  
Keyword(s):  
Joint Pain ◽  
Potential Role ◽  
Monosodium Iodoacetate ◽  
Deficient Mice

scholarly journals Neutral Sphingomyelinase 1 Deficiency in the Mouse Causes No Lipid Storage Disease

2002 ◽  
Vol 22 (11) ◽  
pp. 3633-3638 ◽  
Author(s):  
Markus Zumbansen ◽  
Wilhelm Stoffel
Keyword(s):  
Intracellular Signaling ◽  
Potential Role ◽  
Platelet Activating Factor ◽  
Initial Step ◽  
Lipid Storage Disease ◽  
Neutral Sphingomyelinase ◽  
Mutant Mouse Line ◽  
Deficient Mice ◽  
Null Mutant Mouse

ABSTRACT Sphingomyelin is a major lipid in the bilayer of subcellular membranes of eukaryotic cells. Different sphingomyelinases catalyze the initial step in the catabolism of sphingomyelin, the hydrolysis to phosphocholine and ceramide. Sphingomyelinases have been postulated to generate ceramide as a lipophilic second messenger in intracellular signaling pathways involved in cell proliferation, differentiation, or apoptosis. To elucidate the function of the first cloned Mg2+-dependent, neutral sphingomyelinase (nSMase 1) in sphingomyelin catabolism and its potential role in signaling processes in a genetic and molecular approach, we have generated an nSMase 1-null mutant mouse line by gene targeting. The nSMase 1-deficient mice show an unconspicuous phenotype and no accumulation or changed metabolism of sphingomyelin or other lipids, despite grossly reduced nSMase activity in all organs except brain. We also addressed the recent proposal that nSMase 1 possesses lysophospholipase C activity. The unaltered metabolism of lysophosphatidylcholine or lyso-platelet-activating factor excludes the proposed role of nSMase 1 as a lysophospholipase C.

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