• 2-methoxyestradiol
• coffee
• preeclampsia

• Female
• Animals
• Pregnancy
• 2-Methoxyestradiol/pharmacology
• Pre-Eclampsia/prevention & control
• Rats
• Coffee
• Rats, Sprague-Dawley
• Estradiol/analogs & derivatives
• Estradiol/pharmacology
• Estradiol/blood
• Catechol O-Methyltransferase/metabolism

• HZQB-KCZYB-2020056 Shenzhen-Hong Kong Cooperation Zone for Technology and Innovation
• ZDSYS20190902093417963 Shenzhen Key Laboratory of Steroid Drug Discovery and Development
• JCYJ20190813170607348 Shenzhen Basic Science Project
• 2022E0032 Ganghong Young Scholars Development Fund

• AV fistula
• dialysis access
• endothelium
• inflammation
• smooth muscle cells
• vascular remodeling

• Humans
• Arteriovenous Fistula
• Arteriovenous Shunt, Surgical/adverse effects
• Arteriovenous Shunt, Surgical/methods
• Endothelial Cells
• Renal Dialysis/methods
• Veins/diagnostic imaging
• Veins/surgery
• Veins/pathology
• Female
• Middle Aged

• R01 DK121227 NIDDK NIH HHS
• K08 HL151747 NHLBI NIH HHS
• R01 DK098511 NIDDK NIH HHS
• I01 BX004658 BLRD VA
• R01 DK132888 NIDDK NIH HHS

• Coronary heart disease
• Endothelial progenitor cells
• Inflammation
• Omentin-1
• Restenosis

• Humans
• Animals
• Rats
• Tumor Necrosis Factor-alpha
• Endothelial Progenitor Cells
• Hyperplasia
• Neointima/prevention & control
• Apoptosis
• Carotid Artery Injuries/drug therapy
• Constriction, Pathologic
• Green Fluorescent Proteins

• Blood outgrowth endothelial cells
• EPC characterization
• cardiovascular disease
• food
• nutrients

• Humans
• Cardiovascular Diseases/prevention & control
• Endothelial Progenitor Cells/physiology
• Animals
• Diet, Mediterranean
• Heart Disease Risk Factors
• Biomarkers
• Diet
• Diet, Healthy/methods
• Risk Factors

• cardiology
• heart failure
• preserved ejection fraction
• therapeutics
• translational medicine

• heart failure
• stem cells
• therapy

• CD34+ cells
• TNF-α
• endothelial function
• heart failure

• Age Factors
• Endothelial Progenitor Cells/metabolism
• Heart Failure/metabolism
• Humans
• Inflammation/metabolism
• Interleukin-17/metabolism
• Interleukin-23/metabolism

By low-density lipoprotein (LDL) reduction, statins play an important role in cardiovascular risk modification. Incompletely understood pleiotropic statin effects include vasoprotection that might originate from mobilisation and differentiation of vascular progenitor cells. Data on the potentially differential impact of statin treatment intensity on circulating progenitor cells in patients undergoing percutaneous coronary intervention (PCI) are scarce. This study examines the potential association of different permanent statin treatment regimens on circulating progenitor cells in patients with coronary syndrome.

In a monocentric prospective all-comers study, 105 consecutive cases scheduled for coronary angiography due to either (A) non-invasive proof of ischemia and chronic coronary syndrome (CCS) or (B) troponin-positive acute coronary syndrome (ACS) were included. According to the 2018 American College of Cardiology Guidelines on Blood Cholesterol, patients were clustered depending on their respective permanent statin treatment regimen in either a high- to moderate-intensity statin treatment (HIST) or a low-intensity statin treatment (LIST) group. Baseline characteristics including LDL levels were comparable. From blood drawn at the time of PCI, peripheral blood mononuclear cells were isolated, cultivated and counted and, by density gradient centrifugation, levels of circulating progenitor cells were determined using fluorescence-activated cell sorting (FACS) analysis. In ACS patients both absolute and relative numbers of circulating early-outgrowth endothelial progenitor cells (EPCs) concurrently were significantly lower in the HIST group as compared to the LIST group. This effect was more pronounced in ACS patients than in CCS patients. Both in ACS and CCS patients, HIST caused a significant reduction of the number of circulating SMPCs.

In patients undergoing PCI, a dose intensity-dependent and LDL level-independent pro-differentiating vasoprotective pleiotropic capacity of statins for EPC and SMPC is demonstrated.

• Aerobic training
• Cardiometabolic health
• Cardiovascular disease
• EPC mobilisation
• Endothelial progenitor cells
• Exercise
• Flow cytometry
• High intensity interval training
• Moderate intensity continuous training
• Resistance exercise
• Vascular health

• Endothelial Progenitor Cells
• Endothelium, Vascular
• Exercise/physiology
• Humans
• Metabolic Diseases/metabolism
• Stroke Volume

• Aerobic training
• Cardiometabolic health
• Cardiovascular disease
• EPC mobilisation
• Endothelial progenitor cells
• Exercise
• Flow cytometry
• High intensity interval training
• Moderate intensity continuous training
• Resistance exercise
• Vascular health

• Endothelial Progenitor Cells
• Endothelium, Vascular
• Exercise/physiology
• Humans
• Metabolic Diseases/metabolism
• Stroke Volume

Cardiovascular diseases (CVDs) are the leading cause of death in the world. Endothelial progenitor cells (EPCs) are currently being explored in the context of CVD risk. EPCs are bone marrow derived progenitor cells involved in postnatal endothelial repair and neovascularization. A large body of evidence from clinical, animal, and in vitro studies have shown that EPC numbers in circulation and their functionality reflect endogenous vascular regenerative capacity. Traditionally vitamin D is known to be beneficial for bone health and calcium metabolism and in the last two decades, its role in influencing CVD and cancer risk has generated significant interest. Observational studies have shown that low vitamin D levels are associated with an adverse cardiovascular risk profile. Still, Mendelian randomization studies and randomized control trials (RCTs) have not shown significant effects of vitamin D on cardiovascular events. The criticism regarding the RCTs on vitamin D and CVD is that they were not designed to investigate cardiovascular outcomes in vitamin D-deficient individuals. Overall, the association between vitamin D and CVD remains inconclusive. Recent clinical and experimental studies have demonstrated the beneficial role of vitamin D in increasing the circulatory level of EPC as well as their functionality. In this review we present evidence supporting the beneficial role of vitamin D in CVD through its modulation of EPC homeostasis.

The mobilization of endothelial progenitor cells (EPCs) into circulation from bone marrow is well known to be present in several clinical settings, including acute coronary syndrome, heart failure, diabetes and peripheral vascular disease. The aim of this review was to explore the current literature focusing on the great opportunity that EPCs can have in terms of regenerative medicine.

• EPC
• ischemic heart disease
• progenitor cells

• Biomarker
• DCM
• Diagnosis
• Dilated cardiomyopathy
• Prognosis

• cotransplantation
• myocardial infarction
• myocardial regeneration
• preconditioning
• stem cells

• blood flow
• cardiac hypertrophy
• fatigue
• microcirculation
• skeletal muscle

Takotsubo cardiomyopathy (TCM) is characterized by transient left ventricle dysfunction.

A residual cardiac and endothelial dysfunction is present in patients who recovered from TCM.

In this single‐center prospective study, patients with prior TCM were included and followed for 6.4 ± 1.6 years. All underwent comprehensive cardiac function assessment, including tissue Doppler imaging (TDI) and 2‐dimensional strain (2DS) echocardiography at their first visit. The number of circulating endothelial progenitor cells and levels of proangiogenic vascular endothelial growth factor (VEGF) and its receptor (VEGF‐R) were measured. All measurements were compared with healthy controls.

Forty‐two women (age 58. ±8.6 years, LVEF 58.1 ± 6.1%) comprised the TCM group. Patients post‐TCM had significantly lower early velocities E′ (6 (5.0–8.0) vs. 9 (7.0–11.0) cm/s, p = .001) by TDI and higher E/E′ ratio (p = .002), lower LV global average longitudinal strain (LGS) (−18.9 ± 3.5% vs. −21.7 ± 2.3%, p = .002) and RV LGS (−20.1 ± 3.9% vs. −23.4 ± 2.8%, p = .003) were evident. There was a trend toward a higher VEGF‐R (p = .09) along with decreased VEGF/VEGF‐R ratio representing inadequate VEGF production. In‐hospital mortality was not reported and only two non‐cardiac deaths occurred at long‐term follow‐up.

Altered TDI and 2DS indices suggest residual biventricular myocardial injury in post‐TCM patients with the apparent LV function recovery. Inappropriate production of VEGF and VEGF‐R were observed, suggesting a possible underlying endothelial dysfunction in these patients.

• Takotusubo cardiomyopathy
• endothelial dysfunction
• longitudinal global strain
• tissue Doppler imaging

Numerous reports of vascular events after an initial recovery from COVID-19 form our impetus to investigate the impact of COVID-19 on vascular health of recovered patients. We found elevated levels of circulating endothelial cells (CECs), a biomarker of vascular injury, in COVID-19 convalescents compared to healthy controls. In particular, those with pre-existing conditions (e.g., hypertension, diabetes) had more pronounced endothelial activation hallmarks than non-COVID-19 patients with matched cardiovascular risk. Several proinflammatory and activated T lymphocyte-associated cytokines sustained from acute infection to recovery phase, which correlated positively with CEC measures, implicating cytokine-driven endothelial dysfunction. Notably, we found higher frequency of effector T cells in our COVID-19 convalescents compared to healthy controls. The activation markers detected on CECs mapped to counter receptors found primarily on cytotoxic CD8⁺ T cells, raising the possibility of cytotoxic effector cells targeting activated endothelial cells. Clinical trials in preventive therapy for post-COVID-19 vascular complications may be needed.

• COVID-19
• cell biology
• circulating endothelial cells
• cytokines
• endothelial activation
• human
• immune effector cells
• immunology
• inflammation

Endothelial progenitor cells (EPCs) improve endothelial impairment, which in turn restores endothelial function in patients with heart failure (HF). In the present study, we tested whether fenofibrate, with its anti-inflammatory and vasoprotective effects, could improve myocardial function by activating EPCs through the eNOS pathway in a doxorubicin (DOX)-induced cardiomyopathy mouse model. Wild-type mice were divided into 4 groups and treated with vehicle, DOX + saline, DOX + fenofibrate, and DOX + fenofibrate + L-NAME (N(ω)-nitro-L-arginine methyl ester). DOX-induced cardiac atrophy, myocardial dysfunction, the number of circulating EPCs and tissue inflammation were analyzed. Mice in the DOX + fenofibrate group had more circulating EPCs than those in the DOX + saline group (2% versus 0.5% of total events, respectively) after 4 weeks of treatment with fenofibrate. In addition, the inhibition of eNOS by L-NAME in vivo further abolished the fenofibrate-induced suppression of DOX-induced cardiotoxic effects. Protein assays revealed that, after DOX treatment, the differential expression of MMP-2 (matrix metalloproteinase-2), MMP-9 (matrix metalloproteinase-9), TNF-α (tumor necrosis factor-α), and NT-pro-BNP (N-terminal pro-B-type natriuretic peptide) between saline- and DOX-treated mice was involved in the progression of HF. Mechanistically, fenofibrate promotes Akt/eNOS and VEGF (vascular endothelial growth factor), which results in the activation of EPC pathways, thereby ameliorating DOX-induced cardiac toxicity.

• Aortic valve ectopic calcification
• Aortic valve stenosis
• Tumor necrosis factor-α
• Vascular endothelial growth factor receptor 2
• α-smooth muscle actin

• Biomarkers
• Bone marrow
• Haematopoiesis
• Inflammation
• Myelopoiesis
• Outcomes
• Regeneration
• Stem cells

• Adult
• Cardiovascular Diseases
• Cardiovascular System
• Endothelial Progenitor Cells
• Hematopoiesis
• Hematopoietic Stem Cells
• Humans

• R01 HL137799 NHLBI NIH HHS
• R00 HL122505 NHLBI NIH HHS
• R01 NS064162 NINDS NIH HHS
• P01 HL086773 NHLBI NIH HHS
• R01 HL089650 NHLBI NIH HHS
• P30 DK111024 NIDDK NIH HHS
• U54 AG062334 NIA NIH HHS
• European Foundation for the Study of Diabetes
• Italian Diabetes Society/Lilly 2017
• Cariplo Foundation 2016/0922
• American Heart Association
• Abraham J. and Phyllis Katz Foundation
• National Institute of Health
• NIH

Sarcoidosis is a multisystemic granulomatous disease with still unknown etiology. Our previous studies showed a significantly higher percentage of CD34 + cells in the peripheral blood in patients with sarcoidosis (SA) compared to the control group. The objective of the present study was to characterized of the CD34 + cell population in peripheral blood in patients with SA with reference to the control group. Moreover in patients with SA, fibrocytes and endothelial cells were analysed and their relationship to the fibrosis process based on assessment of diffusing capacity for carbon monoxide (DLCO).

Data from patients diagnosed with SA at Military Institute of Medicine (Warsaw, Poland) between January 2018 and December 2019 were collected and analysed ongoing basis. Peripheral blood was collected from 26 patients with newly diagnosed pulmonary SA and 16 healthy subjects. The immunomagnetic method and flow cytometry were used. Among the CD34+ progenitor cells were assessed: low-differentiated cells, hematopoietic progenitor cells and endothelial progenitor cells. The Statistica 12.0 software was used for a statistical analysis.

We observed a significantly higher percentage of low-differentiated cells (13.8 vs. 2.3, P = 0.001) and endothelial cells (0.3 vs. 0.0, P = 0.001) in patients with SA compared to the control group. In the study group the median proportion of fibrocytes was 1.877% (0.983–2.340) in patients with DLCO< 80%, while in patients with DLCO> 80% was 0.795% (0.139–1.951) (P = 0.72). The median proportion of endothelial progenitor cells was higher in patients with DLCO< 80%: 0.889% (0.391–1.741), than in patients with DLCO> 80%: 0.451% (0.177–0.857) (P = 0.44).

In conclusion we demonstrated for the first time the immunophenotype of peripheral CD34 + cells with the degree of their differentiation. The study confirmed the involvement of low differentiated cells and endothelial cells in patients with SA.

• CD34+ progenitor cells
• Endothelial cells
• Fibrocytes
• Flow cytometry
• Sarcoidosis

• Advanced heart failure
• Chronic heart failure
• LVAD
• Stem cell therapy

Recent studies suggest that circulating endothelial progenitor cells (EPCs) may influence the response to cardiac resynchronization therapy (CRT). The aim of this study was to evaluate the effect of CRT on EPC levels and to assess the impact of EPCs on long-term clinical outcomes.

Prospective study of 50 patients submitted to CRT. Two populations of circulating EPCs were quantified previously to CRT implantation: CD34⁺KDR⁺ and CD133⁺KDR⁺ cells. EPC levels were reassessed 6 months after CRT. Endpoints during the long-term follow-up were all-cause mortality, heart transplantation, and hospitalization for heart failure (HF) management.

The proportion of non-responders to CRT was 42% and tended to be higher in patients with an ischemic vs non-ischemic etiology (64% vs 35%, p = 0.098). Patients with ischemic cardiomyopathy (ICM) showed significantly lower CD34⁺KDR⁺ EPC levels when compared to non-ischemic dilated cardiomyopathy patients (DCM) (0.0010 ± 0.0007 vs 0.0030 ± 0.0024 cells/100 leukocytes, p = 0.032). There were no significant differences in baseline EPC levels between survivors and non-survivors nor between patients who were rehospitalized for HF management during follow-up or not. At 6-month follow-up, circulating EPC levels were significantly higher than baseline levels (0.0024 ± 0.0023 vs 0.0047 ± 0.0041 CD34⁺KDR⁺ cells/100 leukocytes, p = 0.010 and 0.0007 ± 0.0004 vs 0.0016 vs 0.0013 CD133⁺/KDR⁺ cells/100 leukocytes, p = 0.007).

Patients with ICM showed significantly lower levels of circulating EPCs when compared to their counterparts. CRT seems to improve the pool of endogenously circulating EPCs and reduced baseline EPC levels seem not to influence long-term outcomes after CRT.

• Cardiac resynchronization therapy
• Endothelial progenitor cells
• Heart failure
• Prognosis

Behçet's syndrome (BS) is a systemic vasculitis considered as the prototype of a systemic inflammation-induced thrombotic condition whose pathogenesis cannot be explained just by coagulation abnormalities. Circulating hematopoietic progenitor cells (CPC), a population of rare, pre-differentiated adult stem cells originating in the bone marrow and capable of both self-renewal and multi-lineage differentiation, are mobilized in response to vascular injury and play a key role in tissue repair. In cardiovascular and thrombotic diseases, low circulating CPC number and reduced CPC function have been observed. Oxidative stress may be one of the relevant culprits that account for the dysfunctional and numerically reduced CPC in these conditions. However, the detailed mechanisms underlying CPC number reduction are unknown. On this background, the present study was designed to evaluate for the first time the possible relationship between CPC dysfunction and oxidative stress in BS patients. In BS patients, we found signs of plasma oxidative stress and significantly lower CD34+/CD45^−/dim and CD34+/CD45^−/dim/CD133+ CPC levels. Importantly, in all the considered CPC subsets, significantly higher ROS levels with respect to controls were observed. Higher levels of caspase-3 activity in all the considered CPC population and a strong reduction in GSH content in CPC subpopulation from BS patients with respect to controls were also observed. Interestingly, in BS patients, ROS significantly correlated with CPC number and CPC caspase-3 activity and CPC GSH content significantly correlated with CPC number, in all CPC subsets. Collectively, these data demonstrate for the first time that CPC from BS patients show signs of oxidative stress and apoptosis and that a reduced CPC number is present in BS patients with respect to controls. Interestingly, we observed an inverse correlation between circulating CPC number and CPC ROS production, suggesting a possible toxic ROS effect on CPC in BS patients. The significant correlations between ROS production/GSH content and caspase-3 activity point out that oxidative stress can represent a determinant in the onset of apoptosis in CPC. These data support the hypothesis that oxidative-stress-mediated CPC dysfunctioning may counteract their vascular repair actions, thereby contributing to the pathogenesis and the progression of vascular disease in BS.

• Behçet's syndrome
• apoptosis
• circulating progenitor cells
• oxidation
• thrombosis

• AMPK
• Chronic heart failure
• Endothelial progenitor cell
• Fenofibrate
• eNOS

• Biomarkers
• Cardiovascular Diseases/blood
• Cardiovascular Diseases/mortality
• Cell Count
• Female
• Follow-Up Studies
• Hematopoietic Stem Cells/cytology
• Hematopoietic Stem Cells/metabolism
• Humans
• Male
• Mortality
• Odds Ratio
• Patient Outcome Assessment
• Renal Dialysis/adverse effects
• Safety Management

• Japan Society for the Promotion of Science

• Animals
• Antigens, CD34/biosynthesis
• Heart/physiology
• Heart Diseases/therapy
• Humans
• Mice
• Regeneration
• Stem Cell Transplantation
• Stem Cells/metabolism
• Stem Cells/physiology

• 143323 CIHR

• assisted circulation
• heart failure
• stem cells

• Spry1
• angiogenesis
• cell therapy
• culture preconditioning
• ischemia

• Congestive heart failure
• Endothelial dysfunction
• Endothelial progenitor cells

• Acute kidney injury
• Atherosclerosis
• Cardiovascular disease
• Chronic kidney disease
• Endothelial progenitor cells
• Glomerulonephritis
• Microvesicles
• Renal transplantation
• Sepsis

• Animals
• Cardiovascular Diseases/pathology
• Endothelial Progenitor Cells/physiology
• Humans
• Kidney Diseases/pathology

• CD34+ cells
• CD34+VEGFRII+ cells
• Endothelium
• KLOTHO
• Progenitor cells

• Aged
• Antigens, CD34/blood
• Biomarkers/blood
• Cell Count
• Endothelial Progenitor Cells/metabolism
• Female
• Gene Frequency
• Genotype
• Humans
• Klotho Proteins
• Male
• Membrane Proteins/genetics
• Middle Aged
• Phenotype
• Poland
• Polymorphism, Genetic
• Vascular Endothelial Growth Factor Receptor-2/blood

• co-culture
• gene expression
• human endothelial progenitor cells
• in vitro maturation
• oocyte

• cd34⁺ cells
• renin-angiotensin system
• angiotensin-(1-7)
• heart failure

• Angiotensin I/pharmacology
• Antigens, CD34/metabolism
• Case-Control Studies
• Cell Movement/drug effects
• Cells, Cultured
• Female
• Heart Failure/metabolism
• Heart Failure/pathology
• Hematopoietic Stem Cells/drug effects
• Hematopoietic Stem Cells/metabolism
• Hematopoietic Stem Cells/pathology
• Humans
• Male
• Middle Aged
• Nitric Oxide/metabolism
• Peptide Fragments/pharmacology
• Phenotype
• Reactive Oxygen Species/metabolism
• Renin-Angiotensin System/drug effects
• Renin-Angiotensin System/genetics

• R01 HL102033 NHLBI NIH HHS
• UL1 TR001427 NCATS NIH HHS
• R01 HL056921 NHLBI NIH HHS
• UM1 HL087318 NHLBI NIH HHS
• UM1 HL087366 NHLBI NIH HHS

The aim of this review is to discuss recent advances in clinical aspects of stem cell therapy in chronic nonischemic heart failure (DCMP) with emphasis on patient selection, stem cell types, and delivery methods.

Several stem cell types have been considered for the treatment of DCMP patients. Bone marrow-derived cells and CD34⁺ cells have been demonstrated to improve myocardial performance, functional capacity, and neurohumoral activation. Furthermore, allogeneic mesenchymal stem cells were also shown to be effective in improving heart function in this patient population; this may represent an important step towards the development of a standardized stem cell product for widespread clinical use in patients with DCMP.

The trials of stem cell therapy in DCMP patients have shown some promising results, thus making DCMP apparently more inviting target for stem cell therapy than chronic ischemic heart failure, where studies to date failed to demonstrate a consistent effect of stem cells on myocardial performance. Future stem cell strategies should aim for more personalized therapeutic approach by establishing the optimal stem cell type or their combination, dose, and delivery method for an individual patient adjusted for patient's age and stage of the disease.

• CD133+
• CD34+
• CXCR4+
• VEGF
• cardiovascular outcomes
• heart failure
• progenitor cells

• animal model
• dilated cardiomyopathy
• growth factor
• myocardial fibers organization
• neovascularization
• stem cell transplantation

• Cell Survival
• Cell- and Tissue-Based Therapy/trends
• Clinical Trials as Topic
• Humans
• Myocardial Ischemia/therapy
• Stem Cells/metabolism

Endothelial injury is implicated in the pathogenesis of COPD and emphysema; however the role of endothelial progenitor cells (EPCs), a marker of endothelial cell repair, and circulating endothelial cells (CECs), a marker of endothelial cell injury, in COPD and its subphenotypes is unresolved. We hypothesized that endothelial progenitor cell populations would be decreased in COPD and emphysema and that circulating endothelial cells would be increased. Associations with other subphenotypes were examined. The Multi-Ethnic Study of Atherosclerosis COPD Study recruited smokers with COPD and controls age 50–79 years without clinical cardiovascular disease. Endothelial progenitor cell populations (CD34+KDR+ and CD34+KDR+CD133+ cells) and circulating endothelial cells (CD45dimCD31+CD146+CD133-) were measured by flow cytometry. COPD was defined by standard spirometric criteria. Emphysema was assessed qualitatively and quantitatively on CT. Full pulmonary function testing and expiratory CTs were measured in a subset. Among 257 participants, both endothelial progenitor cell populations, and particularly CD34+KDR+ endothelial progenitor cells, were reduced in COPD. The CD34+KDR+CD133+ endothelial progenitor cells were associated inversely with emphysema extent. Both endothelial progenitor cell populations were associated inversely with extent of panlobular emphysema and positively with diffusing capacity. Circulating endothelial cells were not significantly altered in COPD but were inversely associated with pulmonary microvascular blood flow on MRI. There was no consistent association of endothelial progenitor cells or circulating endothelial cells with measures of gas trapping. These data provide evidence that endothelial repair is impaired in COPD and suggest that this pathological process is specific to emphysema.

Type 1 and 2 diabetes decrease the frequencies and functional capacities of circulating angiogenic cells (CAC). Diabetes also elevates gestational complications. These observations may be interrelated. We undertook pilot studies to address the hypothesis that preconception diabetes deviates known gestational increases in CACs. Cross-sectional study of type 1 diabetic, type 2 diabetic and normoglycemic pregnant women was conducted at 1^st, 2^nd, and 3^rd trimester and compared to a 6mo postpartum surrogate baseline. Circulating progenitor cells (CPC; CD34+CD45dimSSlow) and CACs (CD34+CD45dimSSlow expressing CD133 without or with KDR) were quantified by flow cytometry and by colony assay (CFU-Hill). In pregnant normoglycemic women, CD34+CD45dimSSlow cell frequency was greater in 1^st and 3^rd trimester than postpartum but frequency of these cells was static over type 1 or 2 diabetic pregnancies. Type 1 and type 2 diabetic women showed CACs variance versus normal controls. Type 1 diabetic women had more total CD34+KDR+ CACs in 1^st trimester and a higher ratio of CD133+KDR+ to total CD133+ cells in 1^st and 2^nd trimesters than control women, demonstrating an unbalance in CD133+KDR+ CACs. Type 2 diabetic women had more CD133+KDR+ CACs in 1^st trimester and fewer CD133+KDR- CACs at mid-late pregnancy than normal pregnant women. Thus, pregnancy stage-specific physiological fluctuation in CPCs (CD34+) and CACs (CD133+KDR+ and CD133+KDR-) did not occur in type 1 and type 2 diabetic women. Early outgrowth colonies were stable across normal and diabetic pregnancies. Therefore, preconception diabetes blocks the normal dynamic pattern of CAC frequencies across gestation but does not alter colony growth. The differences between diabetic and typical women were seen at specific gestational stages that may be critical for initiation of the uterine vascular pathologies characterizing diabetic gestations.