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Articles by C Weber
Total Records ( 3 ) for C Weber
  C Weber and G. B. Zulian
 

In the case of malignant intestinal obstruction, surgery often carries important mortality and morbidity risks, and feasibility is neither realistic nor reasonable. A total of 4 clinical cases of intestinal obstruction caused by advanced gastrointestinal cancers in their terminal phase are described. The association of analgesics, corticosteroids, antiemetics, and octreotide was effective to relieve symptoms of intestinal obstruction for the remaining lifetime. The insertion of a nasogastric tube was avoided in 3 of 4 cases. Death occurred 51, 56, and 64 days after clinical and radiological diagnosis of irreversible intestinal obstruction. This combination of drugs appears very powerful and well tolerated. The relatively long survival that was observed should encourage future studies of longer half-life somatostatin analogues with no need of continuous infusion or multiple daily injections.

  T Quast , B Tappertzhofen , C Schild , J Grell , N Czeloth , R Forster , R Alon , L Fraemohs , K Dreck , C Weber , T Lammermann , M Sixt and W. Kolanus
 

Adhesion and motility of mammalian leukocytes are essential requirements for innate and adaptive immune defense mechanisms. We show here that the guanine nucleotide exchange factor cytohesin-1, which had previously been demonstrated to be an important component of beta-2 integrin activation in lymphocytes, regulates the activation of the small GTPase RhoA in primary dendritic cells (DCs). Cytohesin-1 and RhoA are both required for the induction of chemokine-dependent conformational changes of the integrin beta-2 subunit of DCs during adhesion under physiological flow conditions. Furthermore, use of RNAi in murine bone marrow DCs (BM-DCs) revealed that interference with cytohesin-1 signaling impairs migration of wild-type dendritic cells in complex 3D environments and in vivo. This phenotype was not observed in the complete absence of integrins. We thus demonstrate an essential role of cytohesin-1/RhoA during ameboid migration in the presence of integrins and further suggest that DCs without integrins switch to a different migration mode.

  P Subramanian , E Karshovska , P Reinhard , R. T. A Megens , Z Zhou , S Akhtar , U Schumann , X Li , M van Zandvoort , C Ludin , C Weber and A. Schober
 

Rationale: The chemokine CXCL12 (CXC motif ligand 12) and its receptor CXCR 4 (CXC motif receptor 4) direct the recruitment of smooth muscle progenitor cells (SPCs) in neointima formation after vascular injury. Lysophosphatidic acid (LPA) induces CXCL12 and neointimal accumulation of smooth muscle cells (SMCs) in uninjured arteries. Thus, we hypothesize that LPA may regulate CXCL12-mediated vascular remodelling.

Objectives: We evaluated the role of LPA receptors in initiating CXCL12-dependent vascular repair by SPCs.

Methods and Results: Wire-induced carotid injury was performed in apolipoprotein E–/– mice on western-type diet. LPA receptor expression was studied by immunostaining and quantitative RT-PCR. LPA receptors LPA1 and LPA3 were detected in the media of uninjured arteries and in the injury-induced neointima. LPA3 mRNA was upregulated and LPA1 mRNA downregulated at one week after injury. The LPA1/3 antagonist Ki16425 inhibited neointima formation by 71% and reduced both relative neointimal SMCs and the macrophage content. Additionally, neointimal hypoxia-inducible factor-1 and CXCL12 expression, the injury-induced peripheral stem cell antigen-1 (Sca-1)+/Lin SPC mobilization, and the neointimal recruitment of Sca-1+SMCs were inhibited by Ki16425. In wild type mice, LPA20:4 increased CXCL12 and hypoxia-inducible factor-1 expression in carotid arteries as early as 1 day following short-term endoluminal incubation. LPA20:4-induced SPC mobilization and neointima formation were blocked by Ki16425, LPA1- and LPA3-specific small interfering (si)RNA, and the CXCR4 antagonist POL5551. Ki16425 reduced LPA20:4-mediated neointimal recruitment of SPC as demonstrated by 2-photon microscopy in bone marrow chimeric mice after repopulation with SM22-LacZ transgenic, hematopoietic cells. Moreover, POL5551 decreased the neointimal accumulation of CXCR4+ SMCs.

Conclusions: LPA1 and LPA3 promote neointima formation through activation of CXCL12-mediated mobilization and recruitment of SPCs.

 
 
 
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