scholarly journals Bone Marrow Endothelial Cells Regulate Myelopoiesis in Diabetes Mellitus

Circulation ◽  
2020 ◽  
Vol 142 (3) ◽  
pp. 244-258 ◽  
Author(s):  
Friedrich Felix Hoyer ◽  
Xinyi Zhang ◽  
Emilie Coppin ◽  
Sathish Babu Vasamsetti ◽  
Ganesh Modugu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Bone Marrow ◽  
Endothelial Cells

scholarly journals Circulating stem and progenitor cells as markers of inflammation, endothelial regeneration, and prediction of vascular complications in metabolic syndrome and type 1 and 2 diabetes mellitus

2018 ◽  
pp. 58-67
Author(s):  
О.В. Першина ◽  
А.В. Пахомова ◽  
Н.Н. Ермакова ◽  
О.Ю. Рыбалкина ◽  
В.А. Крупин ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Syndrome ◽  
Stem Cells ◽  
Bone Marrow ◽  
Endothelial Cells ◽  
Progenitor Cells ◽  
Vascular Complications ◽  
Endothelial Regeneration

Цель исследования состояла в выявлении информативных клеточных маркеров сосудистых осложнений, регенерации микрососудистой сети и воспаления в венозной крови здоровых волонтеров, больных с метаболическим синдромом, сахарным диабетом 1 и 2 типа. Методы. Обследованы больные с метаболическим синдромом (МС), диабетом 2 типа без осложнений, диабетом 1 типа средней степени тяжести и здоровые волонтеры. Диагноз пациентов подтвержден общеклиническими, биохимическими, коагулометрическими и иммуноферментными методами исследования, для оценки экспрессии антигенов использовался многопараметрический цитометрический анализ. Результаты. При анализе экспрессии маркеров показано изменение числа эндотелиальных клеток, мезенхимальных стволовых клеток (МСК) и гемопоэтических стволовых клеток (ГСК) в крови в зависимости от патологии. Эндотелиальные клетки миелоидного (CD45CD14CD34CD309CD144CD31) и немиелоидного (CD45CD14CD34CD309CD144CD31) происхождения, CD309-эндотелиальные клетки и МСК (CD44CD73CD90CD105) предлагаются в качестве маркеров повреждения эндотелия при диабетической симптоматике. При этом ГСК (CD45CD34) могут выступать ценным диагностическим и прогностическим маркером воспаления. Заключение. Для подтверждения сосудистых повреждений и прогноза развития осложнений при диабете 1 и 2 типа в венозной крови пациентов целесообразно оценивать эндотелиальные прогениторные клетки (ЭПК) не костномозговой локализации (CD31CD309CD144) и костномозговой локализации (CD34CD309), и ЭПК c высоким регенеративным потенциалом (CD45CD34CD31CD144). Циркулирующие ЭПК, формирующие колонии in vitro (CD45CD34CD31), рекомендуется использовать в качестве дифференциального маркера состояния регенерации эндотелия при диабете 2 типа. The aim of this study was to identify mesenchymal stem cells (MSC), hematopoietic stem cells (HSC), mature endothelial cells, and endothelial progenitor cells (EPC) in the blood of healthy volunteers, patients with metabolic syndrome, and type 1 and 2 diabetes mellitus as new, informative cellular markers of vascular complications, endothelial regeneration, and inflammation. Methods. The diagnosis was confirmed by general clinical, biochemical, coagulometeric and ELISA studies; multi-parameter cytometric assay was used for evaluation of antigen expression. Results. Changes in the count of MSC, HSC, mature endothelial cells, and endothelial progenitor cells in blood of patients with metabolic syndrome and type 1 and 2 diabetes depended on the type of pathology. We propose using endothelial cells of myeloid (CD45CD14CD34CD309CD144CD31) and non-myeloid origin (CD45CD14CD34CD309CD144CD31), CD309-endothelial cells, and MSCs with the CD44CD73CD90CD105 phenotype as nonspecific markers of endothelial damage in presence of diabetic symptoms. Furthermore, HSCs (CD45CD34) can be used as a valuable diagnostic and prognostic marker of inflammation. Conclusions. It is relevant to evaluate EPCs of non-bone marrow localization (CD31CD309CD144) and bone marrow localization (CD34CD309) and EPCs with a high regenerative potential (CD45CD34CD31CD144) in the blood of patients with type 1 and 2 diabetes to confirm the presence of vascular damage and predict development of complications. Circulating, in vitro colony-forming EPCs (CD45CD34CD31) are recommended as a differential marker for inhibition of endothelial regeneration in type 2 diabetes.

scholarly journals Endothelial-to-mesenchymal transition in lipopolysaccharide-induced acute lung injury drives a progenitor cell-like phenotype

2016 ◽  
Vol 310 (11) ◽  
pp. L1185-L1198 ◽  
Author(s):  
Toshio Suzuki ◽  
Yuji Tada ◽  
Rintaro Nishimura ◽  
Takeshi Kawasaki ◽  
Ayumi Sekine ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Vascular Endothelial Cells ◽  
Repair Process ◽  
Vascular Endothelial ◽  
Mesenchymal Transition ◽  
Oxidase Inhibition ◽  
Endothelial To Mesenchymal Transition

Pulmonary vascular endothelial function may be impaired by oxidative stress in endotoxemia-derived acute lung injury. Growing evidence suggests that endothelial-to-mesenchymal transition (EndMT) could play a pivotal role in various respiratory diseases; however, it remains unclear whether EndMT participates in the injury/repair process of septic acute lung injury. Here, we analyzed lipopolysaccharide (LPS)-treated mice whose total number of pulmonary vascular endothelial cells (PVECs) transiently decreased after production of reactive oxygen species (ROS), while the population of EndMT-PVECs significantly increased. NAD(P)H oxidase inhibition suppressed EndMT of PVECs. Most EndMT-PVECs derived from tissue-resident cells, not from bone marrow, as assessed by mice with chimeric bone marrow. Bromodeoxyuridine-incorporation assays revealed higher proliferation of capillary EndMT-PVECs. In addition, EndMT-PVECs strongly expressed c- kit and CD133. LPS loading to human lung microvascular endothelial cells (HMVEC-Ls) induced reversible EndMT, as evidenced by phenotypic recovery observed after removal of LPS. LPS-induced EndMT-HMVEC-Ls had increased vasculogenic ability, aldehyde dehydrogenase activity, and expression of drug resistance genes, which are also fundamental properties of progenitor cells. Taken together, our results demonstrate that LPS induces EndMT of tissue-resident PVECs during the early phase of acute lung injury, partly mediated by ROS, contributing to increased proliferation of PVECs.

Diabetes mellitus after bone marrow transplantation during childhood

2002 ◽  
Vol 40 (2) ◽  
pp. 128-129 ◽  
Author(s):  
C. Traggiai ◽  
R. Stanhope ◽  
S. Nussey ◽  
A.D. Leiper
Keyword(s):  
Diabetes Mellitus ◽  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Marrow Transplantation

scholarly journals A VCAM-like adhesion molecule on murine bone marrow stromal cells mediates binding of lymphocyte precursors in culture.

1991 ◽  
Vol 114 (3) ◽  
pp. 557-565 ◽  
Author(s):  
K Miyake ◽  
K Medina ◽  
K Ishihara ◽  
M Kimoto ◽  
R Auerbach ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Adhesion Molecule ◽  
Stromal Cells ◽  
Stromal Cell ◽  
Cell Adhesion Molecule ◽  
B Lymphocyte ◽  
Murine Bone Marrow

Two new mAbs (M/K-1 and M/K-2) define an adhesion molecule expressed on stromal cell clones derived from murine bone marrow. The protein is similar in size to a human endothelial cell adhesion molecule known as VCAM-1 or INCAM110. VCAM-1 is expressed on endothelial cells in inflammatory sites and recognized by the integrin VLA-4 expressed on lymphocytes and monocytes. The new stromal cell molecule is a candidate ligand for the VLA-4 expressed on immature B lineage lymphocytes and a possible homologue of human VCAM-1. We now report additional similarities in the distribution, structure, and function of these proteins. The M/K antibodies detected large cells in normal bone marrow, as well as rare cells in other tissues. The antigen was constitutively expressed and functioned as a cell adhesion molecule on cultured murine endothelial cells. It correlated with the presence of mRNA which hybridized to a human VCAM-1 cDNA probe. Partial NH2 terminal amino acid sequencing of the murine protein revealed similarities to VCAM-1 and attachment of human lymphoma cells to murine endothelial cell lines was inhibited by the M/K antibodies. All of these observations suggest that the murine and human cell adhesion proteins may be related. The antibodies selectively interfered with B lymphocyte formation when included in long term bone marrow cultures. Moreover, they caused rapid detachment of lymphocytes from the adherent layer when added to preestablished cultures. The VCAM-like cell adhesion molecule on stromal cells and VLA-4 on lymphocyte precursors may both be important for B lymphocyte formation.

Bone marrow-derived cells are recruited by the melanoma tumor with endothelial cells contributing to tumor vasculature

2016 ◽  
Vol 19 (1) ◽  
pp. 125-133 ◽  
Author(s):  
R. Bonfim-Silva ◽  
L. E. B. Souza ◽  
F. U. F. Melo ◽  
V. C. Oliveira ◽  
D. A. R. Magalhães ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Tumor Vasculature ◽  
Melanoma Tumor ◽  
Bone Marrow Derived Cells

Immortalisation of human bone marrow endothelial cells: characterisation of new cell lines

2000 ◽  
Vol 30 (7) ◽  
pp. 618-629 ◽  
Author(s):  
Rood ◽  
Calafat ◽  
Kr. Von dem Borne ◽  
Gerritsen ◽  
Van Der Schoot
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Cell Lines ◽  
Human Bone ◽  
Human Bone Marrow

scholarly journals Annexin II expressed by osteoblasts and endothelial cells regulates stem cell adhesion, homing, and engraftment following transplantation

Blood ◽  
2007 ◽  
Vol 110 (1) ◽  
pp. 82-90 ◽  
Author(s):  
Younghun Jung ◽  
Jingcheng Wang ◽  
Junhui Song ◽  
Yusuke Shiozawa ◽  
Jianhua Wang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Annexin Ii ◽  
Bone Marrow Niche ◽  
Peptide Fragments ◽  
Hematopoietic Stem ◽  
Marrow Cavity ◽  
Endosteal Niche ◽  
A Cell ◽  
Adhesive Interactions

Differentiation of hematopoietic stem cells (HSCs) after birth is largely restricted to the bone marrow cavity, where HSCs are associated closely with osteoblasts (OBs). How OBs localize HSCs to the endosteal niche remains unclear. To explore adhesive interactions between HSCs and OBs, a cell blot analysis was used that revealed 2 major bands that corresponded to monomers and multimers of annexin II (Anxa2). Immunohistochemistry revealed that OBs and marrow endothelial cells express Anxa2 at high levels. Function-blocking studies confirmed that Anxa2 mediates HSC adhesion mainly via the N-terminal portion of the Anxa2 peptide. Adhesion of HSCs to OBs derived from Anxa2-deficient animals (Anxa2−/−) was significantly impaired compared with OBs obtained from wild-type animals (Anxa2+/+). Moreover, fewer HSCs were found in the marrow of Anxa2−/− versus Anxa2+/+ animals. Short-term lodging, engraftment, and survival of irradiated mice with whole marrow cells were substantially inhibited by N-terminal peptide fragments of Anxa2 or anti-Anxa2 antibodies. Similar findings were noted in long-term competitive repopulation studies. Collectively, these findings reveal that Anxa2 regulates HSC homing and binding to the bone marrow microenvironment and suggest that Anxa2 is crucial for determining the bone marrow niche of HSCs.

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