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Myelofibrosis: molecular and cell biological aspects.

Kreipe H, Büsche G, Bock O, Hussein K - Fibrogenesis Tissue Repair (2012)

Bottom Line: Interestingly, BNIP 3 expression was down regulated in megakaryocytic cell lines kept in hypoxic conditions.Furthermore, expression arrays revealed hypoxia inducible genes to be up-regulated in primary myelofibrosis.Fibrotic MPN are characterized by aberrant proplatelet formation which represent cytoplasmic pseudopodia and normally extend into the sinus.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Pathology, Hannover Medical School, Hannover, Germany.

ABSTRACT
A subset of myeloproliferative disorders (MPN) and myelodyplastic syndromes (MDS) evolves to fibrosis of the bone marrow associated with haematopoietic insufficiency. We have been interested in chemokines involved in fibrogenesis within the bone marrow. Besides TGFβ we could identify a number of additional mediators including osteoprotegerin and bone morphogenic proteins. In MPN JAK2 or MPL mutation are not linked to the propensity for bone marrow fibrosis. The hypothesis that an increased intramedullary decay of megakaryocytes undergoing appotosis takes place within the marrow, thus liberating fibrogenic cytokines, could not be confirmed. On the contrary, megakaryocytes in primary fibrosis revealed low expression of proapoptotic genes such as BNIP3. Interestingly, BNIP 3 expression was down regulated in megakaryocytic cell lines kept in hypoxic conditions. Furthermore, expression arrays revealed hypoxia inducible genes to be up-regulated in primary myelofibrosis. Fibrotic MPN are characterized by aberrant proplatelet formation which represent cytoplasmic pseudopodia and normally extend into the sinus. In fibrotic MPN orientation of proplatelet growth appears to be disturbed, which could lead to an aberrant deposition of platelets in the marrow with consecutive liberation of fibrogenic cytokines.

No MeSH data available.


Related in: MedlinePlus

A-F: Immunohistochemistry for CD42b in ET (A, B), prefibrotic PMF mf0 (C, D) and fibrotic PMF (E, F). Confocal laser microscopy reveals dendritic processes (B, D, F; green staining) whereas in conventional immunohistochemistry predominantly cross sections are seen (brown staining) which increase in density in fibrotic PMF (CD42b; ×400) [17].
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Figure 1: A-F: Immunohistochemistry for CD42b in ET (A, B), prefibrotic PMF mf0 (C, D) and fibrotic PMF (E, F). Confocal laser microscopy reveals dendritic processes (B, D, F; green staining) whereas in conventional immunohistochemistry predominantly cross sections are seen (brown staining) which increase in density in fibrotic PMF (CD42b; ×400) [17].


Myelofibrosis: molecular and cell biological aspects.

Kreipe H, Büsche G, Bock O, Hussein K - Fibrogenesis Tissue Repair (2012)

A-F: Immunohistochemistry for CD42b in ET (A, B), prefibrotic PMF mf0 (C, D) and fibrotic PMF (E, F). Confocal laser microscopy reveals dendritic processes (B, D, F; green staining) whereas in conventional immunohistochemistry predominantly cross sections are seen (brown staining) which increase in density in fibrotic PMF (CD42b; ×400) [17].
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3368793&req=5

Figure 1: A-F: Immunohistochemistry for CD42b in ET (A, B), prefibrotic PMF mf0 (C, D) and fibrotic PMF (E, F). Confocal laser microscopy reveals dendritic processes (B, D, F; green staining) whereas in conventional immunohistochemistry predominantly cross sections are seen (brown staining) which increase in density in fibrotic PMF (CD42b; ×400) [17].
Bottom Line: Interestingly, BNIP 3 expression was down regulated in megakaryocytic cell lines kept in hypoxic conditions.Furthermore, expression arrays revealed hypoxia inducible genes to be up-regulated in primary myelofibrosis.Fibrotic MPN are characterized by aberrant proplatelet formation which represent cytoplasmic pseudopodia and normally extend into the sinus.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Pathology, Hannover Medical School, Hannover, Germany.

ABSTRACT
A subset of myeloproliferative disorders (MPN) and myelodyplastic syndromes (MDS) evolves to fibrosis of the bone marrow associated with haematopoietic insufficiency. We have been interested in chemokines involved in fibrogenesis within the bone marrow. Besides TGFβ we could identify a number of additional mediators including osteoprotegerin and bone morphogenic proteins. In MPN JAK2 or MPL mutation are not linked to the propensity for bone marrow fibrosis. The hypothesis that an increased intramedullary decay of megakaryocytes undergoing appotosis takes place within the marrow, thus liberating fibrogenic cytokines, could not be confirmed. On the contrary, megakaryocytes in primary fibrosis revealed low expression of proapoptotic genes such as BNIP3. Interestingly, BNIP 3 expression was down regulated in megakaryocytic cell lines kept in hypoxic conditions. Furthermore, expression arrays revealed hypoxia inducible genes to be up-regulated in primary myelofibrosis. Fibrotic MPN are characterized by aberrant proplatelet formation which represent cytoplasmic pseudopodia and normally extend into the sinus. In fibrotic MPN orientation of proplatelet growth appears to be disturbed, which could lead to an aberrant deposition of platelets in the marrow with consecutive liberation of fibrogenic cytokines.

No MeSH data available.


Related in: MedlinePlus