Human Umbilical Cord Blood CD34-Positive Cells as Predictors of the Incidence and Short-Term Outcome of Neonatal Hypoxic-Ischemic Encephalopathy: A Pilot Study

Hassanein, Sahar M A; El-Din, Mohamed H; Amer, Hanan; Abdelhamid, Adel; Houssinie, Moustafa El; Ibrahim, Abir

doi:10.3988/jcn.2017.13.1.84

Cited by 4 publications

(4 citation statements)

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“…3a and b. Both CD31 and CD34 are widely used as markers of angiogenesis, hematopoietic cells, and endothelial progenitor cells (Hassanein et al 2017). Thus, the present data are consistent with a role for HDAC4 in both angiogenesis and osteoblast differentiation via regulation of Runx2 and osteocalcin expression (Sun and Beier 2014;Lawson et al 2013).…”

Section: Discussionsupporting

confidence: 87%

Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo

Gao

Wei

et al. 2020

Mol Med

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Background: HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods: HDAC4 was deleted in Col2α1-Cre; HDAC4 fl/fl mice. Growth of the Col2α1-Cre; HDAC4 d/d mice was compared with HDAC4 fl/fl mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results: The Col2α1-Cre; HDAC4 d/d mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; HDAC4 d/d mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. Conclusions: HDAC4 expression in chondrocytes contributes to angiogenesis in the growth plate, and its absence in vivo negatively affects growth plates.

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Section: Discussionsupporting

confidence: 87%

Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo

Gao

Wei

et al. 2020

Mol Med

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“…This process requires a dynamic and close interaction between hypertrophic chondrocytes and vascular invasion. The expressions of typical vascular formation markers, such as CD34 (a widely used marker of hematopoietic and endothelial progenitor cells), were reportedly increased in the tibia of the Hdac4 d/d , col2α1-cre mice (46). The findings of the present study demonstrated that knockout of the HDAC4 gene accelerates endochondral bone formation by promoting vascular invasion.…”

Section: Discussionsupporting

confidence: 60%

Histone deacetylase 4 deletion results in abnormal chondrocyte hypertrophy and premature ossification from collagen type 2α1‑expressing cells

Chen

Sang

et al. 2020

Mol Med Rep

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Histone deacetylase 4 (Hdac4) plays a vital role in chondrocyte hypertrophy and bone formation. To investigate the function of Hdac4 in postnatal skeletal development, the present study developed lineage-specific HDAC4-knockout mice [collagen type 2α1 (col2α1)-cre, Hdac4 d/d mice] by crossing transgenic mice expressing Cre recombinase. Thus, a specific ablation of HDAC4 was performed in col2α1-expressing mice cells. The knee joints of Hdac4 fl/fl and col2α1-cre, Hdac4 d/d mice were analyzed at postnatal day (P)2-P21 using an in vivo bromodeoxyuridine (BrdU) assay, and Safranin O, Von Kossa and whole-body staining were used to evaluate the developmental growth plate, hypertrophic differentiation, mineralization and skeletal mineralization patterns. The trabecular bone was analyzed using microcomputed tomography. The expressions of Brdu, proliferating cell nuclear antigen (Pcna), matrix metalloproteinase (MMP)-13, runt-related transcription factor (runx)-2, osteoprotegerin (oPG), cd34, type X collagen (ColX), osteocalcin and Wnt5a were determined using immunohistochemistry, in situ hybridization (ISH) and reverse transcription-quantitative (rT-q)Pcr. The results demonstrated that Hdac4-null mice (Hdac4 d/d mice) were severely runted; these mice had a shortened hypertrophic zone (histopathological evaluation), accelerated vascular invasion and articular mineralization (Von Kossa staining), elevated expressions of MMP-13, runx2, oPG and cd34 (RT-qPCR and immunohistochemistry), downregulated expression of the proliferative marker Brdu and Pcna (immunohistochemistry), increased expression of colX and decreased expression of Wnt5a (iSH). in conclusion, chondrocyte-derived HDAC4 was responsible for regulating chondrocyte proliferation and differentiation as well as endochondral bone formation.

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“…There were limited data available for neonatal mortality disaggregated by severity of NE. Only 10 reports included data on mortality associated with grade I intrapartum-related NE 37–40 44 45 53–56. In total, 22/236 (9.3%) mild NE cases died.…”

Section: Resultsmentioning

confidence: 99%

Incidence and outcomes of intrapartum-related neonatal encephalopathy in low-income and middle-income countries: a systematic review and meta-analysis

et al. 2022

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AimTo examine the incidence of intrapartum-related neonatal encephalopathy, and neonatal mortality and neurodevelopmental outcomes associated with it in low-income and middle-income countries.MethodsReports were included when neonatal encephalopathy diagnosed clinically within 24 hours of birth in term or near-term infants born after intrapartum hypoxia-ischaemia defined as any of the following: (1) pH≤7.1 or base excess ≤−12 or lactate ≥6, (2) Apgar score ≤5 at 5 or 10 min, (3) continuing resuscitation at 5 or 10 min or (4) no cry from baby at 5 or 10 min. Peer-reviewed articles were searched from Ovid MEDLINE, Cochrane, Web of Science and WHO Global Index Medicus with date limits 1 November 2009 to 17 November 2021. Risk of bias was assessed using modified Newcastle Ottawa Scale. Inverse variance of heterogenicity was used for meta-analyses.ResultsThere were 53 reports from 51 studies presenting data on 4181 children with intrapartum-related neonatal encephalopathy included in the review. Only five studies had data on incidence, which ranged from 1.5 to 20.3 per 1000 live births. Neonatal mortality was examined in 45 studies and in total 636 of the 3307 (19.2%) infants died. Combined outcome of death or moderate to severe neurodevelopmental disability was reported in 19 studies and occurred in 712 out of 1595 children (44.6%) with follow-up 1 to 3.5 years.ConclusionThough there has been progress in some regions, incidence, case mortality and morbidity in intrapartum-related neonatal encephalopathy has been static in the last 10 years.PROSPERO registration numberCRD42020177928.

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Human Umbilical Cord Blood CD34-Positive Cells as Predictors of the Incidence and Short-Term Outcome of Neonatal Hypoxic-Ischemic Encephalopathy: A Pilot Study

Cited by 4 publications

References 36 publications

Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo

Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo

Histone deacetylase 4 deletion results in abnormal chondrocyte hypertrophy and premature ossification from collagen type 2α1‑expressing cells

Incidence and outcomes of intrapartum-related neonatal encephalopathy in low-income and middle-income countries: a systematic review and meta-analysis

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