an-efficient-method-to-obtain-dedifferentiated-fat-cells

An Efficient Method to Obtain Dedifferentiated Fat Cells

Tissue engineering and cell therapy hold great promise clinically. In this regard, multipotent cells, such as mesenchymal stem cells (MSCs), may be used ...

Nihon University

We experienced two rare cases of mismatch between the results of FFR and myocardial perfusion SPECT for identification of myocardial ischemia after myocardial infarction. If a FFR cutoff value of 0.75 is applied as in angina patients to patients with myocardial infarction, the severity of ischemia may be underestimated.

Mismatch between results of myocardial fractional flow reserve (FFR) measurements and myocardial perfusion SPECT for identification of the severity of ischemia: pitfall of FFR in patients with prior myocardial infarction.

Bone marrow cells implantation (BMI) has been reported to efficiently improve ischemic heart disease. However, BMI strategies are generally invasive. To establish a BMI strategy for ischemic heart disease, we performed implantation of autologous cryopreserved mononuclear cells (MNCs) from bone marrow (BM) retrogradely into the myocardium via the coronary vein in pigs with acute myocardial infarction (AMI) and old myocardial infarction (OMI).

A strategy of retrograde injection of bone marrow mononuclear cells into the myocardium for the treatment of ischemic heart disease.

Bronchoesophageal fistulae associated with lymphomas are generally associated with chemo-radiotherapy. We report here an unusual case of lymphoma with a therapy-unrelated bronchoesophageal fistula. Previously, only 10 similar cases have been reported. A 70-year-old male was diagnosed as having gastric diffuse large B-cell lymphoma in May 1998. In January 1999, he noted a cough after eating and drinking. Because of the presence of a febrile temperature, productive cough and dyspnea, he was referred to our hospital and diagnosed as having aspiration pneumonia. Antibiotics did not improve his symptoms. When tracheal intubation was performed with bronchoscopy, a bronchoesophageal fistula was revealed. Malignant lymphoma cells were found around the fistula in the biopsy specimen. The patient died of pneumonia after treatment with airway stenting and chemotherapy. Induction of necrosis by chemotherapy or low blood flow with stenting and dopamine probably caused enlargement of the fistula.

[Bronchoesophageal fistula in a patient with untreated malignant lymphoma].

Although granulocyte colony-stimulating factor (G-CSF) has been shown to prevent cardiac remodeling after acute myocardial infarction, the mechanism and safety of G-CSF treatment acute myocardial infarction remain controversial. The purpose of the present study was to investigate in a rat model the mechanisms underlying the beneficial effect of G-CSF in acute myocardial infarction and to determine whether G-CSF treatment aggravates vascular remodeling of injured artery after acute myocardial infarction. Sprague-Dawley rats received transplanted bone marrow cells from green fluorescent protein (GFP) transgenic rats. Acute myocardial infarction was induced by ligation of the left coronary artery. After 24 h, the right carotid artery was injured with a balloon catheter. G-CSF (100 microg/kg/day) or saline was injected subcutaneously for 5 consecutive days after induction of acute myocardial infarction. G-CSF treatment significantly improved left ventricle function and reduced infarct size in rats with acute myocardial infarction. Expression of mRNA for the angiogenic cytokines was significantly higher in the infarction border area in the G-CSF group than in the control group. The surviving cardiomyocytes in infarction area were more in the G-CSF group. GFP-positive cells were gathered in the infarction border area in both groups; G-CSF did not increase cardiac homing of GFP-positive bone marrow cells in contrast to control group. Most GFP-positive cells were CD68-positive (macrophages). It was difficult to find bone marrow-derived cardiomyocytes in the infarcted area. G-CSF treatment inhibited neointima formation and increased reendothelialization of the injured artery. GFP-positive cells were identified most in the adventitia of the injured artery. A few cells in the neointima and reendothelialization were GFP positive. In conclusion, administration of G-CSF appears to be effective for treatment of left ventricular remodeling after acute myocardial infarction and does not aggravate vascular remodeling. The effect of G-CSF on cardiac and vascular remodeling may occur mainly through a direct action on the heart and arteries.

Effects of G-CSF on cardiac remodeling and arterial hyperplasia in rats.

Although the use of drug-eluting stents (DESs) has been shown to limit neointima hyperplasia, currently available DESs may adversely affect reendothelialization, possibly precipitating cardiac events. We evaluated the effect of an antisense oligodeoxynucleotide (ODN) targeted to the platelet-derived growth factor (PDGF) A-chain on in-stent restenosis in pig coronary artery.

Stent-based delivery of antisense oligodeoxynucleotides targeted to the PDGF A-chain decreases in-stent restenosis of the coronary artery.

Although transplantation of mononuclear cells (MNCs) induces angiogenesis in myocardial infarction, transplantation requires a large amount of bone marrow or peripheral blood cells. We examined the effects of transplantation of peripheral MNCs expressing an exogenous vascular endothelial growth factor (VEGF) gene in a pig model of acute myocardial infarction (AMI).

Low invasive angiogenic therapy for myocardial infarction by retrograde transplantation of mononuclear cells expressing the VEGF gene.

Angiogenesis, the process by which new blood vessels arise from preexisting ones, is critical for embryonic development and is an integral part of many disease processes. Recent studies have provided detailed information on how angiogenic sprouts initiate, elongate, and branch, but less is known about how these processes cease. Here, we show that S1PR1, a receptor for the blood-borne bioactive lipid sphingosine-1-phosphate (S1P), is critical for inhibition of angiogenesis and acquisition of vascular stability. Loss of S1PR1 leads to increased endothelial cell sprouting and the formation of ectopic vessel branches. Conversely, S1PR1 signaling inhibits angiogenic sprouting and enhances cell-to-cell adhesion. This correlates with inhibition ofÂ vascular endothelial growth factor-A (VEGF-A)-induced signaling and stabilization of vascular endothelial (VE)-cadherin localization at endothelial junctions. Our data suggest that S1PR1 signaling acts as a vascular-intrinsic stabilization mechanism, protecting developing blood vessels against aberrant angiogenic responses.

Article	Year
Mismatch between results of myocardial fractional flow reserve (FFR) measurements and myocardial perfusion SPECT for identification of the severity of ischemia: pitfall of FFR in patients wi... Japanese heart journal\| PubMed ID: 15557728	2004
A strategy of retrograde injection of bone marrow mononuclear cells into the myocardium for the treatment of ischemic heart disease. Journal of molecular and cellular cardiology\| PubMed ID: 16271723	2006
[Bronchoesophageal fistula in a patient with untreated malignant lymphoma]. [Rinshō ketsueki] The Japanese journal of clinical hematology\| PubMed ID: 16440767	2005
Effects of G-CSF on cardiac remodeling and arterial hyperplasia in rats. European journal of pharmacology\| PubMed ID: 16979158	2006
Stent-based delivery of antisense oligodeoxynucleotides targeted to the PDGF A-chain decreases in-stent restenosis of the coronary artery. Journal of cardiovascular pharmacology\| PubMed ID: 17086098	2006
Low invasive angiogenic therapy for myocardial infarction by retrograde transplantation of mononuclear cells expressing the VEGF gene. International journal of cardiology\| PubMed ID: 19167769	2010
The sphingosine-1-phosphate receptor S1PR1 restricts sprouting angiogenesis by regulating the interplay between VE-cadherin and VEGFR2. Developmental cell\| PubMed ID: 22975327	2012

Kazuhiro Hagikura

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