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Background—
Adult stem cells can contribute to myocardial regeneration after ischemic injury. Bone marrow and skeletal muscles contain a population of CXCR4
+
cells expressing genes specific for muscle progenitor cells that can be mobilized into the peripheral blood. The aims of the study were (1) to confirm the presence of early tissue-committed cells expressing cardiac, muscle, and endothelial markers in populations of mononuclear cells in peripheral blood and (2) to assess the dynamics and magnitude of the mobilization of CD34
+
, CD117
+
, CXCR4
+
, c-met
+
, CD34/CD117
+
, and CD34/CXCR4
+
stem cells into peripheral blood in relation to inflammatory and hematopoietic cytokines in patients with ST-segment–elevation acute myocardial infarction (STEMI).
Methods and Results—
Fifty-six patients with STEMI (<12 hours), 39 with stable angina, and 20 healthy control subjects were enrolled. Real-time reverse transcription–polymerase chain reaction (RT-PCR) was used for detection of tissue-specific markers. The number of the cells was assessed by use of a flow cytometer on admission, after 24 hours, and after 7 days. RT-PCR revealed increased expression of mRNA (up to 3.5-fold increase) for specific cardiac (GATA4, MEF2C, Nkx2.5/Csx), muscle (Myf5, Myogenin, MyoD), and endothelial (VE-cadherin, von Willebrand factor) markers in peripheral blood mononuclear cells. The number of CD34/CXCR4
+
and CD34/CD117
+
and c-met
+
stem cells in peripheral blood was significantly higher in STEMI patients than in stable angina and healthy subjects, peaking on admission, without further significant increase after 24 hours and 7 days.
Conclusions—
The study demonstrates in the setting of STEMI a marked mobilization of mononuclear cells expressing specific cardiac, muscle, and endothelial markers as well as CD34/CXCR4
+
and CD34/CD117
+
and c-met
+
stem cells and shows that stromal cell–derived factor-1 is an important factor influencing the mobilization.
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original articleT h e ne w e ngl a nd jou r na l o f m e dic i ne n engl j med 360;19 nejm.org
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