Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mesenchymal stem cells (MSCs) are the most promising seed cells for cell therapy and tissue engineering, which can be isolated from various sources of human adult tissues such as bone marrow and adipose tissue. However, cells from these tissues must be obtained through invasive procedures and sometimes the individual difference is hard to control. Hence, the search continues for an ethically conducive, easily accessible and controllable source of stem cells. We herein report the isolation of a population of stem cells from the human placental decidua basalis (termed as PDB-MSCs), a maternal portion of placenta. PDB-MSCs were further shown to express markers common to MSCs and positive for SSEA-1, SSEA-3, SSEA-4, TRA-1-60, TRA-1-81 and Oct-4. In order to facilitate the further utility in ischemic diseases, we tested the apoptosis of PDB-MSCs in hypoxia and serum deprivation, two components of ischemia in vivo. Taken together, our findings indicate that PDB-MSCs are resistant to hypoxia and serum deprivation, which may relate to Bcl-2.
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PMID:Isolation of mesenchymal stem cells from human placental decidua basalis and resistance to hypoxia and serum deprivation. 1959 Sep 88

The idea of antiangiogenesis as a therapeutic strategy has been around for several decades (1). Vigorously pursued as a novel anticancer strategy (reviewed in (2-6), it is now widely considered to be a promising approach to the treatment of a range of pathologies of which uncontrolled vascular proliferation is a component (see Table 1). To date, therapeutic benefit has been achieved with antiangiogenic therapy in the treatment of life-threatening infantile hemangioma, pulmonary hemangiomatosis, and in the treatment of some vascular tumors (7,8). Table 1 Table 1 Pathologies Likely to Benefit from Therapeutic Intervention in Angiogenesis Excess angiogenesis Insufficient angiogenesis Arthritis Angiology Inflammatory, Vascular malformation Rheumatoid, Hemifacial micromia Kaposi's sarcoma Bone fracture nonunion Leukemia, lymphoma, and myeloma Chronic wounds Macular degeneration Ischemia/infarction Paget's disease Cerebral Psoriasis Intestinal Retinopathy (and its vascular complications) Myocardial Proliferative Peripheral Of prematurity Pyrogenic granuloma Solid carcinomas Ulcer Primary Duodenal Secondary (metastasis) Gastric Vascular tumors Hemangioma Capillary Juvenile (infantile) Hemangiomatosis Hemagioblastoma Other benign vascular proliferations.
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PMID:Therapeutic inhibition of angiogenesis. 2134 Sep 8

Valosin-containing protein (VCP) is a highly expressed member of the type II AAA+ ATPase family. VCP mutations are the cause of inclusion body myopathy, Paget's disease of the bone, and frontotemporal dementia (IBMPFD) and they account for 1%-2% of familial amyotrophic lateral sclerosis (ALS). Using fibroblasts from patients carrying three independent pathogenic mutations in the VCP gene, we show that VCP deficiency causes profound mitochondrial uncoupling leading to decreased mitochondrial membrane potential and increased mitochondrial oxygen consumption. This mitochondrial uncoupling results in a significant reduction of cellular ATP production. Decreased ATP levels in VCP-deficient cells lower their energy capacity, making them more vulnerable to high energy-demanding processes such as ischemia. Our findings propose a mechanism by which pathogenic VCP mutations lead to cell death.
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PMID:Pathogenic VCP mutations induce mitochondrial uncoupling and reduced ATP levels. 2356 33


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