Cell Systems
Human Primary Cells
Cell Systems에서는 Human 조직에서 분리되어 계대배양이 가능한 Primary cell을 제공합니다.
제품 소개
Cell Systems의 Primary Cell 제품은 인간 세포 기반 연구 및 생명 과학 분야에서 혁신적인 도구로 활용됩니다. 폐, 간, 피부, 혈관 등 다양한 인체 조직에서 유래한 1차 세포를 제공하며, 세포의 생리학적 특성을 최대한 유지하여 연구의 신뢰성을 높입니다. Cell Systems만의 엄격한 품질 관리 기준과 자체적으로 개발한 분리/추출 기술을 통해 최상의 생존율과 재현성을 보이는 Primary cell을 보장하며, 다양한 질환 모델링과 정상 상태를 포함한 광범위한 연구 목적에 적합한 솔루션을 제공합니다.
- 높은 생존율과 재현성을 보이며, 계대배양이 가능한 Human Primary Cell
- 폐, 간, 피부, 혈관 등 다양한 조직 유래 세포로 폭넓은 연구 가능
- 수천 건 이상의 SCI 문헌 인용 횟수
- 세포 성장 및 배양을 위한 맞춤형 배지와 시약 제공
| Category | Category # | Cell Type |
| Eye | ACBRI 181 | Retinal Microvascular Endothelial Cells |
| ACBRI 183 | Retinal Pericyte Cells | |
| Brain | ACBRI 376 | Brain Microvascular Endothelial Cells |
| ACBRI 498 | Brain Pericytes | |
| Liver | ACBRI 566 | Liver Sinusoidal Microvascular Endothelial Cells |
| Kidney | ACBRI 127 | Glomerular Mesangial Cells |
| ACBRI 128 | Glomerular Microvascular Endothelial Cells | |
| Lung | ACBRI 468 | Lung Microvascular Endothelial Cells |
| ACBRI 469 | Lung Fibroblast Cells | |
| Heart | ACBRI 375 | Aortic Endothelial Cells |
| ACBRI 716 | Aortic Smooth Muscle Cells | |
| ACBRI 377 | Coronary Artery Endothelial Cells | |
| ACBRI 443 | Coronary Artery Smooth Muscle Cells | |
| ACBRI 5118 | Cardiac Fibroblast Cells | |
| CSC 2A0 | Arterial Endothelial Cells (Pooled) | |
| CSC 2SM3 | Vascular Smooth Muscle Cells (Pooled) | |
| HuVEC | CSC 2V0 | Venous Endothelial Cells (HUVEC) |
| Dermal | ACBRI 539 | Dermal Microvascular Endothelial Cells |
| ACBRI 2K0 | Keratinocytes | |
| CSC 2F0 | Dermal Fibroblast Cells (Pooled) | |
| CSC 2M1 | Dermal Microvascular Endothelial Cells | |
| Intestine | ACBRI 666 | Large Intestine Microvascular Endothelial Cells |
| Other | ACBRI 134 | Pancreatic Microvascular Endothelial Cells |
| ACBRI 3733 | Prostate Microvascular Endothelial Cells | |
| CSC 2HM1 | Melanocyte Cells (Pooled) | |
| ACBRI 488 | Synovial Microvascular Endothelial Cells | |
| ACBRI 479 | Synovial Stromal Cells | |
| Bovine | CSC 2B2 | Primary Bovine Aortic Endothelial Cells (Pooled) |
데이터 자료
Fig1. Immunofluorescence Staining of Primary Human Retinal Microvascular Endothelial Cells (ACBRI 181) Showing LDL Expression (>95% Positive)
Fig2. Immunofluorescence Staining of Primary Human Brain Microvascular Endothelial Cells (ACBRI 376) Demonstrating CD31 Expression (>98% Positive)
Fig3. Morphology of Primary Human Vascular Smooth Muscle Cells (Pooled) (CSC 2SM3) at Passage 4, 4 Days Post-Plating
추천대상
다양한 장기의 혈관세포로 연구 효율이 높아졌어요
대학 생명공학과
여러 장기의 혈관세포를 손쉽게 구할 수 있어서 실험 디자인과 진행이 매우 편리했습니다. 다양한 모델에 활용할 수 있어 효율적입니다.
Organ-on-a-Chip 모델에 사용하기 편리
바이오텍
별다른 분화과정 없이 배양 후 바로 이용하면 되어서 진행이 빨라졌습니다
BBB 모델링
대학교 연구실
다수의 SCI 문헌에서 인용되어 BBB 모델링 관련하여 참고할 만한 자료가 많아 연구 설계와 실험 진행이 수월했습니다.
Publication (3)
Retinoblastoma is the most common intraocular malignancy in children with poor prognosis. The progression of retinoblastoma is dependent on a robust angiogenic response. Targeting both retinoblastoma cells and angiogenesis may therefore provide an alternative therapeutic strategy in retinoblastoma. Here, we demonstrated the inhibitory effects of tigecycline, a FDA-approved antibiotic, in retinoblastoma and angiogenesis in vitro and in vivo. We showed that tigecycline significantly inhibited growth and induced caspase-dependent apoptosis of multiple retinoblastoma cell lines. Tigecycline also effectively inhibited angiogenesis through suppressing capillary network formation, migration, proliferation and survival of human retinal microvascular endothelial cell (HREC). Mechanistically, tigecycline acts on both retinoblastoma cells and HREC via inhibiting mitochondrial protein translation, resulting in mitochondrial dysfunction, energy crisis, and oxidative damage. Importantly, we demonstrated the in vivo efficacy of tigecycline in inhibiting retinoblastoma and angiogenesis, and inducing oxidative stress on xenograft mouse model. In addition, ATP levels and growth rates were largely affected in retinoblastoma ρ0 cells that lacked mitochondrial respiration. Our work provides systematic pre-clinical evidence for repurposing tigecycline from its traditional use for retinoblastoma treatment. Our work demonstrates the essential roles of mitochondrial metabolism in both retinoblastoma and its angiogenesis.
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Emerging clinical data suggests that ~40% of COVID-19 patients develop neurological symptoms attributed to viral encephalitis, resulting in neuro-inflammation, neuronal damage and severe hypoxia (Wu et al. 2020; Najjar et al. 2020; Muccioli et al. 2020; Mao et al. 2020). SARS-COV-2 infects the host using the widely expressed angiotensin converting enzyme 2 (ACE2) receptor (Bourgonje et al. 2020), however, no there are no reports on ACE2 receptor expression by human brain microvascular endothelial cells (BMVEC) and normal human astrocytes (NHA) which constitute the Blood Brain Barrier (BBB). We posit that SARS-CoV-2 enters the central nervous system (CNS) via ACE2 receptors present on BMVEC and NHA, alters tight junction (TJ) proteins leading to disruption in BBB integrity which leads to neuro-invasion of microglia. Overall, SARS-COV-2 exacerbates neuro-inflammation, increases oxidative stress and consequently contributes to neuronal cell death.
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One important function of endothelial cells in glioblastoma multiforme (GBM) is to create a niche that helps promote self-renewal of cancer stem-like cells (CSLC). However, the underlying molecular mechanism for this endothelial function is not known. Since activation of NOTCH signaling has been found to be required for propagation of GBM CSLCs, we hypothesized that the GBM endothelium may provide the source of NOTCH ligands. Here, we report a corroboration of this concept with a demonstration that NOTCH ligands are expressed in endothelial cells adjacent to NESTIN and NOTCH receptor-positive cancer cells in primary GBMs. Coculturing human brain microvascular endothelial cells (hBMEC) or NOTCH ligand with GBM neurospheres promoted GBM cell growth and increased CSLC self-renewal. Notably, RNAi-mediated knockdown of NOTCH ligands in hBMECs abrogated their ability to induce CSLC self-renewal and GBM tumor growth, both in vitro and in vivo. Thus, our findings establish that NOTCH activation in GBM CSLCs is driven by juxtacrine signaling between tumor cells and their surrounding endothelial cells in the tumor microenvironment, suggesting that targeting both CSLCs and their niche may provide a novel strategy to deplete CSLCs and improve GBM treatment.
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Human Primary Cells