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M Trojanowska

Publications and source records attributed to M Trojanowska.

51 records · Page 3Linked to original sources
PubMed1981

Microbial short-term assays with thiram in vitro.

The fungicide thiram was assayed in the following tests in vitro, with and without metabolic activation: (1) prophage lambda induction of Escherichia coli K12; (2) repair test in Salmonella typhimurium (strains TA1538 and TA1978); (3) induction of gene mutations in Aspergillus nidulans (methA1 suppressor induction). Thiram was positive in the repair test and in the A. nidulans forward-mutation test (4-6 fold increase) in the absence of metabolic activation. A slight increase was observed in prophage lambda induction with thiram in the presence of the metabolic activation system.

Aspergillus nidulans↗
PubMedDate not supplied

The 72-kilodalton IE-1 protein of human cytomegalovirus (HCMV) is a potent inducer of connective tissue growth factor (CTGF) in human dermal fibroblasts.

Latent human cytomegalovirus (HCMV) infection has been implicated in diseases characterized by tissue remodeling. Because of recent evidence indicating the possibility of a partial HCMV reactivation, the purpose of this study was to examine the role of the HCMV immediate early (IE) genes in the regulation of extracellular matrix (ECM) related host genes. Adenoviral vector expressing IE1 was generated to allow efficient gene delivery into human fibroblasts. IE1 stimulated the prolonged expression of connective tissue growth factor (CTGF) and TIMP1. IE1-dependent stimulation of CTGF was partially mediated by TGF-beta. Moreover, whereas collagenous proteins and collagen type 1 mRNA were only transiently induced by IE1 in the majority of fibroblasts, in selected fibroblast strains IE1 induced persistent ECM upregulation for up to 120 hours. This study suggests that transient or limited HCMV reactivation may play a direct role in abnormal matrix remodeling in GVHD, scleroderma, atherosclerosis and other HCMV-linked diseases.

Cell Culture Techniques↗
PubMedDate not supplied

What did we learn by studying scleroderma fibroblasts?

Systemic sclerosis (SSc, scleroderma) is a complex disease manifesting itself by fibrosis of skin and other internal organs. Fibroblasts isolated from SSc lesions and cultured in vitro are characterized by the increased synthesis of collagen and other extracellular matrix (ECM) proteins, consistent with the disease phenotype. Cultured SSc fibroblasts therefore serve as a principal experimental model for studying the molecular and cellular mechanisms involved in collagen overproduction in this disease. This article provides an overview of transcription factors that are deregulated in SSc fibroblasts. The possible origin of SSc fibroblasts is also discussed.

Collagen↗