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Smoothelin

About: Smoothelin is a research topic. Over the lifetime, 264 publications have been published within this topic receiving 14069 citations.


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Journal ArticleDOI
TL;DR: A rare spontaneous hepatic leiomyosarcoma with osteOSarcomatous differentiation was observed in a female beagle dog and its morphological and immunohistochemical characteristics were examined.
Abstract: A rare spontaneous hepatic leiomyosarcoma with osteosarcomatous differentiation was observed in a female beagle dog and its morphological and immunohistochemical characteristics were examined. Upon necropsy, an endoceliac mass originating from the liver was detected, which was composed of hematoid fluid-filled cysts and white to grayish solid tissue. There were no macroscopic findings in other organ systems. Histopathologically, the hepatic mass consisted of two different mesenchymal components. One form was spindle cells arranged in interlacing fascicles immunohistochemically positive for smooth muscle actin (SMA) and smoothelin, indicating leiomyosarcomatous differentiation. The other form was composed of short spindle cells positive for S-100 and was producing various amounts of eosinophilic osteoid and trabecula-like matrices positive for osteocalcin, indicating osteosarcomatous differentiation. In addition, invasive growth in the hepatic parenchyma and cell atypia were observed. Based on these findings, the mass was diagnosed as hepatic leiomyosarcoma with osteosarcomatous differentiation (malignant mesenchymoma), which might be derived from undifferentiated mesenchymal cells.

2 citations

Journal ArticleDOI
TL;DR: In this paper, a swine model of catheter dysfunction and bloodstream infection is presented to serve as a platform to develop therapeutic innovations for this important clinical problem. But, the model is not suitable for large-scale clinical trials.
Abstract: Background Although tunneled dialysis catheters (TDC) are far from ideal, they still represent the main form of vascular access for most patients beginning dialysis. Catheters are easy to place and allow patients instant access to dialysis, but regardless of these benefits, catheters are associated with a high incidence of significant complications like bloodstream infections, central venous stenosis, thrombosis, and dysfunction. In the present study, we aim to describe and characterize a swine model of catheter dysfunction and bloodstream infection, that recreates the clinical scenario, to help to serve as a platform to develop therapeutic innovations for this important clinical problem. Methods Six Yorkshire cross pigs were used in this study. Non-coated commercial catheters were implanted in the external jugular recreating the main features of common clinical practice. Catheters were aseptically accessed twice a week for a mock dialysis procedure (flushing in and out) to assess for and identify catheter dysfunction. Animals were monitored daily for infections; once detected, blood samples were collected for bacterial culture and antibiograms. Study animals were euthanized when nonresponsive to treatment. Tissue samples were collected in a standardized fashion for macroscopic inspection and histological analysis. Results The data analysis revealed an early onset of infection with a median time to infection of 9 days, 40% of the isolates were polymicrobial, and the average time to euthanasia was 20.16 ± 7.3 days. Median time to catheter dysfunction onset was 6 days post-implantation. Postmortem dissection revealed external fibrin sheath and internal thrombosis as the main causes of catheter dysfunction. There was also evidence of central venous stenosis with positive cells for αSMA, CD68, Ki67, Smoothelin, and Vimentin within the venous neointima. Conclusions The described model represents a reliable and reproducible large animal model of catheter dysfunction and bloodstream infection, which recreates all the main complications of TDC's and so could be used as a validated large animal model to develop new therapies for TDC related infection, thrombosis/dysfunction and central venous stenosis.

2 citations

Journal ArticleDOI
14 Aug 2021-Cells
TL;DR: The authors used bead-immobilized Jagged1 to direct phenotype control of primary human coronary artery smooth muscle cells (HCASMC) and to differentiate embryonic multipotent mesenchymal progenitor (10T1/2) cell towards a vascular lineage.
Abstract: In Notch signaling, the Jagged1-Notch3 ligand-receptor pairing is implicated for regulating the phenotype maturity of vascular smooth muscle cells. However, less is known about the role of Jagged1 presentation strategy in this regulation. In this study, we used bead-immobilized Jagged1 to direct phenotype control of primary human coronary artery smooth muscle cells (HCASMC), and to differentiate embryonic multipotent mesenchymal progenitor (10T1/2) cell towards a vascular lineage. This Jagged1 presentation strategy was sufficient to activate the Notch transcription factor HES1 and induce early-stage contractile markers, including smooth muscle α-actin and calponin in HCASMCs. Bead-bound Jagged1 was unable to regulate the late-stage markers myosin heavy chain and smoothelin; however, serum starvation and TGFβ1 were used to achieve a fully contractile smooth muscle cell. When progenitor 10T1/2 cells were used for Notch3 signaling, pre-differentiation with TGFβ1 was required for a robust Jagged1 specific response, suggesting a SMC lineage commitment was necessary to direct SMC differentiation and maturity. The presence of a magnetic tension force to the ligand-receptor complex was evaluated for signaling efficacy. Magnetic pulling forces downregulated HES1 and smooth muscle α-actin in both HCASMCs and progenitor 10T1/2 cells. Taken together, this study demonstrated that (i) bead-bound Jagged1 was sufficient to activate Notch3 and promote SMC differentiation/maturation and (ii) magnetic pulling forces did not activate Notch3, suggesting the bead alone was able to provide necessary clustering or traction forces for Notch activation. Notch is highly context-dependent; therefore, these findings provide insights to improve biomaterial-driven Jagged1 control of SMC behavior.

2 citations

Book ChapterDOI
TL;DR: Elucidation of the cellular and molecular mechanisms regulating the development and differentiation of the SMC lineage provides fundamental insights into smooth muscle cell biology and the unique capacity of this muscle cell lineage to respond to injury and adapt to environmental stress.
Abstract: Smooth muscle cells (SMCs) are responsible for the coordination of physiologic processes required for maintenance of organismal homeostasis ranging from the regulation of vascular tone and airway mechanics to digestion and elimination. The unique capacity of SMCs to modulate their phenotype from a contractile to a synthetic cell is attributable to the dynamic regulation of the SMC lineage-restricted genes, including SM-α-actin, SM-myosin heavy chain, SM22α, calponin, telokin, and smoothelin. The expression of these genes is regulated, and modulated, by the myocardin family of transcriptional coactivators. The lineage relationships that define and distinguish functionally distinct subsets of vascular and visceral SMCs remain poorly understood. The embryologic origins of SMCs are complex and include both mesodermally and ectodermally derived progenitors that hone to specific locations throughout the body where they differentiate and subserve distinct functions. The differentiation and specification of SMCs from stem and progenitor cells involves interplay between extracellular matrix components, integrins and the timed expression of transcription factors and their co-activators. Elucidation of the cellular and molecular mechanisms regulating the development and differentiation of the SMC lineage provides fundamental insights into smooth muscle cell biology and the unique capacity of this muscle cell lineage to respond to injury and adapt to environmental stress.

2 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202113
202012
20196
20188
201713
20165