• Title/Summary/Keyword: Angiogenic capacity

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Expression of the C1orf31 Gene in Human Embryonic Stem Cells and Cancer Cells

  • Ahn, Jin-Seop;Moon, Sung-Hwan;Yoo, Jung-Ki;Jung, Hyun-Min;Chung, Hyung-Min;Kim, Jin-Kyeoung
    • Reproductive and Developmental Biology
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    • v.32 no.4
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    • pp.223-227
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    • 2008
  • Human embryonic stem (ES) cells retain the capacity for self-renewal, are pluripotent and differentiate into the three embryonic germ layer cells. The regulatory transcription factors Oct4, Nanog and Sox2 play an important role in maintaining the pluripotency of human ES cells. The aim of this research was to identify unknown genes upregulated in human ES cells along with Oct4, Nanog, and Sox2. This study characterizes an unknown gene, named chromosome 1 open reading frame 31 (C1orf31) mapping to chromosome 1q42.2. The product of C1orf31 is the hypothetical protein LOC388753 having a cytochrome c oxidase subunit VIb (COX6b) motif. In order to compare expression levels of C1orf31 in human ES cells, human embryoid body cells, vascular angiogenic progenitor cells (VAPCs), cord-blood endothelial progenitor cells (CB-EPCs) and somatic cell lines, we performed RT-PCR analysis. Interestingly, C1orf31 was highly expressed in human ES cells, cancer cell lines and SV40-immortalized cells. It has a similar expression pattern to the Oct4 gene in human ES cells and cancer cells. Also, the expression level of C1orf31 was shown to be upregulated in the S phase and early G2 phase of synchronized HeLa cells, leading us to purpose that it may be involved in the S/G2 transition process. For these reasons, we assume that C1orf31 may play a role in on differentiation of human ES cells and carcinogenesis.

Cell-Assisted Lipotransfer for the Treatment of Parry-Romberg Syndrome

  • Castro-Govea, Yanko;De La Garza-Pineda, Oscar;Lara-Arias, Jorge;Chacon-Martinez, Hernan;Mecott-Rivera, Gabriel;Salazar-Lozano, Abel;Valdes-Flores, Everardo
    • Archives of Plastic Surgery
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    • v.39 no.6
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    • pp.659-662
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    • 2012
  • Progressive facial hemiatrophy, also known as Parry-Romberg syndrome, is a progressive and self-limited deformation of the subcutaneous tissue volume on one side of the face that creates craniofacial asymmetry. We present the case of a patient with a five-year history of progressive right facial hemiatrophy, who underwent facial volumetric restoration using cell-assisted lipotransfer (CAL), which consists of an autologous fat graft enriched with adipose-derived stem cells (ASCs) extracted from the same patient. ASCs have the capacity to differentiate into adipocytes. They also promote angiogenesis, release angiogenic growth factors, and some can survive as stem cells. The use of autologous fat as a filler in soft tissue atrophy has been satisfactory in patients with mild and moderate Parry-Romberg syndrome. Currently, CAL has showed promising results in the long term by decreasing the rate of fat reabsorption. The permanence and stability of the graft in all the injected areas has showed that autologous fat grafts enriched with stem cells could be a promising technique for the correction of defects caused by this syndrome.

Comparative histomorphologic study of regenerated bone for dental implant placement in the atrophied posterior maxilla

  • Kim, Se-Jung;Kim, Soung-Min;Kim, Ji-Hyuck;Park, Young-Wook
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.33 no.1
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    • pp.28-39
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    • 2007
  • The purpose of this study is to evaluate the regenerative capacity of reconstruction in the atrophied posterior maxilla by comparing bone graft procedures and alveolar distraction osteogenesis (ADO) techniques. We performed the autogenous iliac bone graft (AGB group, 5 specimens in 3 patients), and the combination (Mixed group, 3 specimens in 3 patients) of the autogenous and deproteinized bovine bone ($Bio-Oss^{(R)}$, Geistlich Co., Switzerland) as the ratio of 2:1 in the sinus floor elevation procedures. ADO procedures using $TRACK^{(R)}$ (KLS Martin Co., Germany) were also performed to augment vertical alveolar height in atrophied posterior maxilla (ADO group, 5 specimens in 4 patients). Newly generated bone tissues were obtained with the 2.0mm diameter trephine bur (3i Co., USA) during implant fixture installation after 5-7 months. Routine histolomorphological observation, immunodot blot assay for quantitative evaluation, and immunohistochemical staining with antibodies to MMP-1, -9, -10, TIMP-1, -2, and BMP-2, -4 were all carried out. Lamellar bone formation was well shown in all specimens and new bone formations of ADO group increased than those of other procedures. In immunohistochemical staining, the strong expression of BMP-2 was shown in all specimens, and immunodot blot assay showed that bone formation is accompanied by the good induction of factors associated with angiogenesis and appeared more increased amount of osteogenic and angiogenic factors in ADO group. ADO is the most effective technique for new bone formation compared to sinus floor elevation with autogenous or mixed bone graft in the atrophied posterior maxilla. In the quantitative immunodot blot assay, the regenerated bone after ADO showed more increased products of VEGF, BMP-2, PCNA and MMP-1 than those after the other procedures, and these findings were able to be confirmed by immunohistochemical stainings.

Recombinant human KAI1/CD82 attenuates M1 macrophage polarization on LPS-stimulated RAW264.7 cells via blocking TLR4/JNK/NF-κB signal pathway

  • Hyesook Lee;Jung-Hwa Han;Kangbin An;Yun Jeong Kang;Hyun Hwangbo;Ji Hye Heo;Byung Hyun Choi;Jae-Joon Kim;Seo Rin Kim;Soo Yong Lee;Jin Hur
    • BMB Reports
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    • v.56 no.6
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    • pp.359-364
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    • 2023
  • KAI1/CD82, a membrane tetraspanin protein, can prevent various cancers and retinal disorders through its anti-angiogenic and anti-metastatic capacity. However, little is known about its anti-inflammatory effect and molecular mechanism. Therefore, the present study aimed to inLPSvestigate effect of a recombinant protein of the large extracellular domain of human KAI1 (Gly 111-Leu 228, rhKAI1) on lipopolysaccharides (LPS)-stimulated RAW264.7 macrophage-like cells and mouse bone marrow-derived macrophages (BMDM) and to identify its underlying mechanism. Our data showed that rhKAI1 suppressed expression levels of classically macrophages (M1) phenotype-related surface markers F4/80+CD86+ in LPS-stimulated BMDM and RAW264.7 cells. In addition, LPS markedly increased mRNA expression and release levels of pro-inflammatory cytokines and mediators such as interleukin (IL)-1β, IL-6, tumor necrosis factor-α, cyclooxygenase-2, nitric oxide and prostaglandin E2, whereas these increases were substantially down-regulated by rhKAI1. Furthermore, LPS strongly increased expression of NF-κB p65 in the nuclei and phosphorylation of ERK, JNK, and p38 MAPK. However, nuclear translocation of NF-κB p65 and phosphorylation of JNK were greatly reversed in the presence of rhKAI1. Especially, rhKAI1 markedly suppressed expression of toll-like receptor (TLR4) and prevented binding of LPS with TLR4 through molecular docking predict analysis. Importantly, Glu 214 of rhKAI1 residue strongly interacted with Lys 360 of TLR4 residue, with a binding distance of 2.9 Å. Taken together, these findings suggest that rhKAI1 has an anti-inflammatory effect on LPS-polarized macrophages by interacting with TLR4 and down-regulating the JNK/NF-κB signaling pathway.