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Клетки эндотелия легочной артерии человека: HPAEC. Первичные клеточные линии Cell Applications.

Human Pulmonary Artery Endothelial Cells: HPAEC

Клетки Эндотелия Легочной Артерии (HPAEC) предоставляют прекрасную модельную систему для изучения многих аспектов сердечно-сосудистых функций и заболеваний, включая связанные с диабетом расстройства, механизмы эндотелиальной дисфункции, вызыванные условиями окружающей среды, оксидативным стрессом, гипоксией и воспалением, а также способов действия различных природных соединений и потенциальных лекарств.

HPAEC от Cell Applications использовались для:

(Текст на языке оригинала)
  • Investigate vasculoprotective effects of propofol and show tat it induces Angiotensin-converting enzyme 2(ACE2) transcription via a PI3K-dependent mechanism, demonstrating its potential for treating pulmonary arterial hypertension
  • Analyze hits from a high-throughput screening assay and discover anziaic acid, from the lichen Hypotrachyna sp., as novel inhibitor for both Y. pestis and E. coli topoisomerase I
  • Show that endothelin-1 that is released by endothelial cells during acute crisis in sickle cell anemia, increases vascular constriction
  • Demonstrate that pollutant particles cause vascular dysfunction by up-regulating clotting-related genes, such as F2RL2, FOS, JUN, NF-kB, F2RL2, HMOX1 and tissue factor F3-mediated increase in IL-6 and IL-8 and activation of NADPH oxidase
  • Demonstrate the central role of AMP-activated protein kinase (AMPK) in normal endothelial barrier function that is disrupted by exposure to lipopolysaccharides inhibiting AMPK, and causing endothelial hyperpermeability and lung injury
  • Confirm anti-inflammatory and cardioprotective effects of resveratrol by showing that it suppresses IL-13 and TNF-α induced eotaxin-1 gene expression, inhibits expression of JAK-1, reduces STAT6 phosphorylation and decreases p65 subunit of NF-κB
  • Determine that cGMP can prevent oxidant-induced damage to the endothelial barrier function by activating cGMP-dependent protein kinase PKGI through a Ca2+ independent mechanism
  • Demonstrate that exposure to radiation causes endothelial cells senescence (as judged by induction, downstream of mTOR, of senescence markers p53, p21/waf1, and senescence-associated b-Gal) due to up-regulation of proliferative signaling (IGF-1 and IGF-2 and hyperphosphorylation of IGF-1R) in the presence of cell cycle arrest
  • Show that vanadium exposure causes pulmonary vasoconstriction mediated in part by the inhibition of endothelial NO production via PKC-dependent phosphorylation of Thr495 of eNOS
  • Evaluate, along with Human Dermal Microvascular Endothelial Cells (CADMEC) and Human Umbilical Cord Vascular Endothelial Cells (HUVEC), all obtained от Cell Applications, Inc., the cytotoxic effects of a novel pore-forming protein, proposed as an anti-tumor agent
  • Compare effects of BMP-4 on HPAEC and Human Coronary Artery Endothelial Cells (HCAEC, also от Cell Applications, Inc.) and showing that only in HCAEC BMP-4 treatment induced ROS, activated NF-kB, ICAM-1 and increased monocyte adhesiveness, explaining why its upregulation leads to atherosclerosis and hypertension in the systemic, but not pulmonary circulation
  • Demonstrate that macro- , but not micro-vascular pulmonary endothelial cells accumulate HIF-1 under hypoxic conditions
  • Confirm SPNS2 role as a transporter for S1P, a bioactive lipid, by monitoring S1P release from HPAEC and Human Umbilical Vein Endothelial Cells, both obtained от Cell Applications, Inc., and by showing that S1P was not released when SPNS2 was silenced with siRNA. Additionally, quantitative real-time PCR indicated that Spns2 mRNA was transcribed at higher levels in venous HUVEC compared to arterial HPAEC, suggesting heterogeneity in the expression level of SPNS2 among different vascular beds.

Обратите внимание, что некоторые публикации описывают разницу между эндотелиальными клетками из разных сосудистых русел и между макро- и микрососудистыми клетками из одного органа, подчеркивая важность подтверждения каких-либо новых результатов, полученных на клеточных лотах, полученных из других источников. Cell Applications, Inc. предлагает широчайшее разнообразие эндотелиальных клеток и хорошо подготовлены для  удовлетворения этой потребности.


Normal human pulmonary artery. Each lot is tested negative for HIV, Hepatitis B, Hepatitis C, mycoplasma, bacteria, and fungi.
Cryopreserved ampoule:
2nd passage, >500,000 cells in Basal Medium containing 10% FBS & 10% DMSO.
Kit contains:
Ampoule of cryopreserved HPAEC (302-05a), 500 ml of Endothelial Cell Media (211-500), and a Subculture Reagent Kit (090K).
Proliferating Cells:
Shipped in Growth Medium at 3rd passage in either flasks or multiwell dishes.
Population doublings:
Can be cultured at least 15 doublings



Cheng, B., S. Cao, V. Vasquez, T. Annamalai, G. Tamayo-Castillo, J. Clardy, and Y.-C. Tse-Dinh. 2013. Identification of Anziaic Acid, a Lichen Depside from Hypotrachyna sp., as a New Topoisomerase Poison Inhibitor. PloS one. 8:e60770.
Panganiban, R.A.M., and R.M. Day. 2013. Inhibition of IGF-1R Prevents Ionizing Radiation-Induced Primary Endothelial Cell Senescence. PloS one. 8:e78589.
Xing, J., Q. Wang, K. Coughlan, B. Viollet, C. Moriasi, and M.-H. Zou. 2013. Inhibition of AMP-Activated Protein Kinase Accentuates Lipopolysaccharide-Induced Lung Endothelial Barrier Dysfunction and Lung Injury in Vivo. Am. J. pathology. 182:1021-1030.
Cao, L., L. Xu, B. Huang, and L. Wu. 2012. Propofol Increases Angiotensin-Converting Enzyme 2 Expression in Human Pulmonary Artery Endothelial Cells. Pharmacology. 90:342-347.
Hisano, Y., N. Kobayashi, A. Yamaguchi, and T. Nishi. 2012. Mouse SPNS2 Functions as a Sphingosine-1-Phosphate Transporter in Vascular Endothelial Cells. PloS one. 7:e38941.
Yang, C.J., C.Y. Lin, T.-c. Hsieh, S.C. Olson, and J.M. Wu. 2011. Control of eotaxin-1 expression and release by resveratrol and its metabolites in culture human pulmonary artery endothelial cells. American journal of cardiovascular disease. 1:16.
Karoly, E.D., Z. Li, L.A. Dailey, X. Hyseni, and Y.-C.T. Huang. 2007. Up-regulation of tissue factor in human pulmonary artery endothelial cells after ultrafine particle exposure. Environmental health perspectives. 115:535.
Fujiuchi, S., Y. Yamazaki, Y. Fujita, Y. Nishigaki, A. Taked, Y. Yamamoto, T. Fijikane, T. Shimizu, S. Osanai, T. Takahashi, and K. Kikuchi. 2006. S-Nitrosoglutathione (SNOG) Accumulates Hypoxia Inducible Factor-1α in Main Pulmonary Artery Endothelial Cells but not in Micro Pulmonary Vessel Endothelial Cells. In THE ARTERIAL CHEMORECEPTORS. Vol. 580. Y. Hayashida, C. Gonzalez, and H. Kondo, editors. Springer US. 63-71.
Li, Z., X. Hyseni, J.D. Carter, J.M. Soukup, L.A. Dailey, and Y.-C.T. Huang. 2006. Pollutant particles enhanced H2O2 production from NAD (P) H oxidase and mitochondria in human pulmonary artery endothelial cells. American Journal of Physiology-Cell Physiology. 291:C357-C365.
Moldobaeva, A., L.E. Welsh-Servinsky, L.A. Shimoda, R.S. Stephens, A.D. Verin, R.M. Tuder, and D.B. Pearse. 2006. Role of protein kinase G in barrier-protective effects of cGMP in human pulmonary artery endothelial cells. Am. J. Physiol. 290:L919-L930.
Li, Z., J. Carter, L. Dailey, and Y. Huang. 2005. Pollutant Particles Produce Vasoconstriction and Enhance MAPK Signaling via Angiotensin Type 1 Receptor. Environmental Health Perspectives, 113:1009.
Ergul, S., C.Y. Brunson, J. Hutchinson, A. Tawfik, A. Kutlar, R.C. Webb, and A. Ergul. 2004. Vasoactive factors in sickle cell disease: In vitro evidence for endothelin-1-mediated vasoconstriction. American Journal of Hematology. 76:245-251.
Li, Z., J.D. Carter, L.A. Dailey, and Y.C. Huang. 2004. Vanadyl sulfate inhibits NO production via threonine phosphorylation of eNOS. Environmental health perspectives. 112:201-206.

For general cryopreservation of most primary cells. Contains FBS & DMSO. 040-50 6228.74 руб.

HPAEC Total Kit: Media, Subculture Reagents & Cells, Adult 302K-05a 94552.78 руб.

Cryopreserved HPAEC 302-05a 77236.91 руб.

25 x 24-Well Rxns TF101KS 6222.62 руб.
250 x 24-Well Rxns TF101K 49829.91 руб.

Basal medium (contains no growth supplement).В  Add GS before use. 210-500 8097.09 руб.
Basal medium without growth supplement and phenol red 210PR-500 8720.1 руб.

Basal medium & growth supplement sold together packaged separately 211K-500 14326.51 руб.

Starvation medium without phenol red 209PR-250 9093.77 руб.
Use when cells need to be starved overnight to 24 hrs before experiment 209-250 8097.09 руб.

Total RNA prepared from human heart tissue 1H30-50 16039.28 руб.
Total RNA prepared from human heart tissue 1H30-250 60419.04 руб.

Total RNA prepared from Human Pulmonary Artery Endothelial Cells, adult 302-R10a 40486.8 руб.
Total RNA prepared from Human Pulmonary Artery Endothelial Cells, adult 302-R25a 80974.29 руб.

Proliferating HPAEC 303-25a 77236.91 руб.
Proliferating HPAEC 303-75a 100906.53 руб.
Proliferating HPAEC 303-6Wa 100906.53 руб.
Proliferating HPAEC 303-96Wa 115855.36 руб.

100 ml each of HBSS, Trypsin/EDTA & Trypsin Neutralizing Solution 090K 6353.07 руб.

Extended Family Products

100 tests 028-S 4152.49 руб.
500 tests 028-01 16070.53 руб.

Related Products

Defined medium without serum 113-500 13080.49 руб.
Defined medium without serum and phenol red 113PR-500 13703.5 руб.

All-in-one ready-to-use 211-500 12208.14 руб.
Growth medium without antibiotics 211A-500 13080.49 руб.
Growth medium without FBS 211F-500 13080.49 руб.
Growth medium without hydrocortisone 211H-500 13080.49 руб.
Growth medium without phenol red 211PR-500 13080.49 руб.

Added to Basal Medium to create Growth Medium 211-GS 6602.41 руб.
Growth supplement without antibiotics 211A-GS 7848.43 руб.
Growth supplement without FBS 211F-GS 8097.09 руб.
Growth supplement without hydrocortisone 211H-GS 7848.43 руб.

Информация представлена исключительно в ознакомительных целях и ни при каких условиях не является публичной офертой