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C Magnus Sköld

Publications and source records attributed to C Magnus Sköld.

6 recordsLinked to original sources
PubMed2003

Platelets stimulate fibroblast-mediated contraction of collagen gels.

BACKGROUND: Platelets are thought to play a role in a variety of inflammatory conditions in the lung, some of which may lead to fibrosis. In the current study we tested the hypothesis that whole platelets and platelet lysate can mediate remodelling of extracellular matrix in vitro by affecting fibroblast-mediated contraction of a collagen gel. We also sought to determine to what extent platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) contribute to this effect. METHODS: Washed platelets, isolated from healthy blood donors, and platelet lysate (freezing and thawing), were cast together with human lung fibroblasts in three-dimensional collagen gels. The gels were then released and cultured for four days. PDGF and TGF-beta1 concentrations were measured in culture supernatants by ELISA. RESULTS: Both platelets and platelet lysate augmented fibroblast-mediated gel contraction in a time and concentration dependent manner (19.9% +/- 0.1 (mean +/- SEM) of initial area vs. 48.0% +/- 0.4 at 48 hours; P < 0.001 and 41.5% +/- 0.6 vs. 60.6% +/- 0.3 at 48 hours; P < 0.001, respectively). Fixed platelets had no effect in the system. Both TGF-beta1 and PDGF-AA/AB were released in co-culture. PDGF-AA/AB had a maximum release at 24 hours whereas TGF-beta1 release increased with longer culture periods. Neutralising antibodies to these mediators partially inhibited platelet-induced gel contraction. CONCLUSION: We conclude that platelets may promote remodelling of extracellular matrix in vitro and that PDGF and TGF-beta partially mediate this effect, also indicating a role for other mediators. The findings may be an important mechanism in regulating repair processes after injury.

Antibodies↗
PubMed2003

Glucocorticoids modulate TGF-beta production by human fetal lung fibroblasts.

TGF-beta1 is thought to play a central role in pulmonary fibrosis inducing fibroblast differentiation and extracellular matrix synthesis. In human lung fibroblasts, it is still unclear how various TGF-beta isoforms affect TGF-beta production and whether glucocorticoids, commonly used agents to treat fibrotic lung disease, modulate these processes. To this end, human fetal lung fibroblasts (HFLF) were cultured with various concentrations of glucocorticoids (budesonide, dexamethasone or hydrocortisone) with and without TGF-beta1, -beta2, or -beta3. Post-culture media were collected for ELISA assays of TGF-beta1, -beta2, and -beta3. TGF-beta mRNA was assessed by real time RT-PCR. Smad 2, 3, and 4 and AP-1 complex (c-fos and c-Jun) cellular localization were evaluated by immunostaining. TFG-beta2 and -beta3 stimulated TGF-beta1 production significantly (p < 0.01 relative to control). TGF-beta1 stimulated TGF-beta2 production (p < 0.01 relative to control). TGF-beta3 was undetectable. Glucocorticoids significantly inhibited TGF-beta1 and TGF-beta2 production and reduced expression of the up-regulated TGF-beta1 and TGF-beta2 mRNA induced by exogenous TGF-beta1, -beta2, or -beta3 (p < 0.01 for each) but had no effect on Smads. Although c-jun-related nuclear staining was not intensified in TGF-beta-stimulated cells, it was reduced by glucocorticoids. Thus, TGF-beta isoforms may stimulate production of various TGF-beta isoforms in the lung. Glucocorticoids then may block TGF-beta production by modulating mRNA levels and c-Jun.

Cells, Cultured↗
PubMed2002

Glucocorticoids modulate TGF-beta production.

TGF-beta is thought to play a central role in pulmonary fibrosis inducing fibroblast differentiation and extracellular matrix synthesis. In human lung fibroblasts, it is still unclear how various TGB-beta isoforms affect TGF-beta production and whether glucocorticoids, commonly used agents to treat fibrotic lung disease, modulate these processes. To this end, human fetal lung fibroblasts (HFL-1) were cultured with various concentrations of glucocorticoids (budesonide, dexamethasone or hydrocortisone) with and without TFG-beta1, -beta2, and -beta3. TGF-beta mRNA was assessed by real time RT-PCR. Smad 2, 3, and 4 and AP-1 complex (c-fos and c-Jun) cellular localization were evaluated by immunostaining. TGF-beta2 and -beta3 stimulated TGF-beta1 production significantly (p < 0.01 relative to control). TGF-beta1 stimulated TGF-beta2 production (p < 0.01 relative to control). TGF-beta3 was undetectable. Glucocorticoids significantly inhibited TGF-beta1 and -beta2 production and reduced expression of the upregulated TGF-beta1 and -beta2 mRNA induced by exogenous TGF-beta1, -beta2 or -beta3 (p < 0.01 for each) but had no effect on Smads. Although c-jun-related nuclear staining was not intensified in TGF-beta-stimulated cells, it was reduced by glucocorticoids. Thus, TGF-beta isoforms may stimulate production of various TGF-beta isoforms in the lung. Glucocorticoids then may block TGF-beta production by modulating mRNA levels and c-Jun.

Animals↗
PubMedDate not supplied

Coccidioidomycosis mimicking lung cancer.

A 65-year-old female smoker was admitted due to haemoptysis and a pulmonary infiltrate in the right lower lung lobe. Tumour was suspected, but there was also a history of 2 years spent in Arizona, known to be endemic for the dimorphic fungus Coccidioides immitis. IgG antibodies and airway culture for C. immitis were negative, and surgery was performed for suspected lung cancer. No malignancy was detected at histopathological investigation, but typical coccidioidal spherulae were observed by silver stain. Coccidioidoma may be a differential diagnosis to malignant tumour in individuals visiting endemic areas.

Aged↗
PubMedDate not supplied

Pulmonary epithelioid hemangioendothelioma: report of a case with fine needle aspiration biopsy.

BACKGROUND: Pulmonary epithelioid hemangioendothelioma (PEH) is a rare, low grade, malignant vascular tumor that typically presents with multiple pulmonary nodules in young women. This report details the cytopathologic and pathologic findings in an unusual case presenting in an older male with a pleural effusion, dominant nodule and multiple bilateral infiltrates. CASE: A 62-year-old, male nonsmoker was referred due to increasing dyspnea. Chest radiography revealed a pleural effusion and nodular infiltrate in the right upper lobe of the bronchus. Thoracocentesis and thoracoscopy were performed, with a pleural drain inserted. Bronchoscopy revealed a right upper lobe bronchus occluded by a greyish, necrotic mass. Various cytopathologic sampling techniques, including fine needle aspiration biopsy, as well as traditional histopathologic biopsies were performed. Cytologic specimens showed loosely cohesive, epithelioid cells that were binucleated and multinucleated. Chromatin was granular, with scattered, small, multiple nucleoli with occasional, variably sized cytoplasmic vacuoles. The patient's condition deteriorated, and he died 3 weeks after admission. CONCLUSION: Pulmonary epithelioid hemangioendotheliomas are unusual neoplasms with a epithelioid, discohesive cellular appearance. It can mimic other, more commonly seen pulmonary neoplasms. Careful attention to cytomorphologic features and application of ancillary studies assist in making the diagnosis.

Biopsy, Fine-Needle↗