产品号 #05513_C
用于培养小鼠间充质干细胞和骨髓间充质干细胞
You may notice that your reagent packaging looks slightly different from images displayed here or from previous orders. Due to pandemic-related plasticware shortages, we are temporarily using alternative bottles for this product. Rest assured that the products themselves and how you should use them have not changed.
Products for Your Protocol
To see all required products for your protocol, please consult the Protocols and Documentation.
-
3% Acetic Acid with Methylene BlueReagent for manual counting of nucleated mammalian cells
-
L-GlutamineCell culture supplement
-
Trypsin-EDTA (0.25%)Enzymatic cell dissociation reagent
-
EasySep™ BufferCell separation buffer
概述
MesenCult™扩增试剂盒（小鼠）是标准的小鼠间充质间质细胞（MSCs）培养；也称为间充质干细胞)和小鼠胚胎成纤维细胞（mef）。该试剂盒包括MesenCult™基础培养基（小鼠），MesenCult™10X补充（小鼠）和MesenPure™。MesenCult™扩增培养基已经过优化，可用于小鼠MSCs和mef的体外衍生和扩增，以及集落形成单位-成纤维细胞（CFU-F）的检测。该试剂盒使用小鼠菌株C57BL/6的细胞进行优化。
为了促进MSCs和mef在细胞培养过程中的富集，无需连续传代和频繁的培养基变化，只需在使用前添加MesenPure™以完成MesenCult™扩增培养基。虽然不是必需的，但强烈建议添加MesenPure™，因为与单独使用完整的mesenult™扩增培养基相比，所得到的MSC和MEF培养物更均匀，并且表现出更强大的增殖、分化和集落形成。
注意：MesenCult™膨胀介质必须补充l -谷氨酰胺（目录#07100）。
Subtype
Specialized Media
Cell Type
Mesenchymal Stem and Progenitor Cells, Mouse Embryonic Fibroblasts
Species
Mouse
Application
Cell Culture, Colony Assay, Expansion
Brand
MesenCult
Area of Interest
Stem Cell Biology
Data Figures
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Resources and Publications
Educational Materials (5)
Publications (16)
Loss of KDM4B exacerbates bone-fat imbalance and mesenchymal stromal cell exhaustion in skeletal aging. Cell stem cell 2021 feb
Abstract
Skeletal aging is a complex process, characterized by a decrease in bone formation, an increase in marrow fat, and stem cell exhaustion. Loss of H3K9me3, a heterochromatin mark, has been proposed to be associated with aging. Here, we report that loss of KDM4B in mesenchymal stromal cells (MSCs) exacerbated skeletal aging and osteoporosis by reducing bone formation and increasing marrow adiposity via increasing H3K9me3. KDM4B epigenetically coordinated $\beta$-catenin/Smad1-mediated transcription by removing repressive H3K9me3. Importantly, KDM4B ablation impaired MSC self-renewal and promoted MSC exhaustion by inducing senescence-associated heterochromatin foci formation, providing a mechanistic explanation for stem cell exhaustion with aging. Moreover, while KDM4B was required for parathyroid hormone-mediated bone anabolism, KDM4B depletion accelerated bone loss and marrow adiposity induced by a high-fat diet. Our results suggest that the epigenetic rejuvenation and reversing bone-fat imbalance might be new strategies for preventing and treating skeletal aging and osteoporosis by activating KDM4B in MSCs.
Aging-Related Reduced Expression of CXCR4 on Bone Marrow Mesenchymal Stromal Cells Contributes to Hematopoietic Stem and Progenitor Cell Defects. Stem cell reviews and reports 2020 may
Abstract
Aging impairs the regenerative potential of hematopoietic stem cells (HSC) and skews differentiation towards the myeloid lineage. The bone marrow (BM) microenvironment has recently been suggested to influence HSC aging, however the mechanisms whereby BM stromal cells mediate this effect is unknown. Here we show that aging-associated decreased expression of CXCR4 expression on BM mesenchymal stem cells (MSC) plays a crucial role in the development of the hematopoietic stem and progenitor cells (HSPC) aging phenotype. The BM MSC from old mice was sufficient to drive a premature aging phenotype of young HSPC when cultured together ex vivo. The impaired ability of old MSC to support HSPC function is associated with reduced expression of CXCR4 on BM MSC of old mice. Deletion of the CXCR4 gene in young MSC accelerates an aging phenotype in these cells characterized by increased production of reactive oxygen species (ROS), DNA damage, senescence, and reduced proliferation. Culture of HSPC from young mice with CXCR4 deficient MSC also from young mice led to a premature aging phenotype in the young HSPC, as evidenced by reduced hematopoietic regeneration and enhanced myeloid differentiation. Mechanistically, CXCR4 signaling prevents BM MSC dysfunction by suppressing oxidative stress, as treatment of old or CXCR4 deficient MSC with N-acetyl-L-cysteine (NAC), improved their niche supporting activity, and attenuated the HSPC aging phenotype. Our studies suggest that age-associated reduction in CXCR4 expression on BM MSC impairs hematopoietic niche activity with increased ROS production, driving an HSC aging phenotype. Thus, modulation of the SDF-1/CXCR4 axis in MSC may lead to novel interventions to alleviate the age-associated decline in immune/hematopoietic function.
Increased yield of gelatin coated therapeutic cells through cholesterol insertion. Journal of biomedical materials research. Part A 2020 jun
Abstract
Gelatin coatings are effective in increasing the retention of MSCs injected into the heart and minimizing the damage from acute myocardial infarction (AMI), but early studies suffered from low fractions of the MSCs coated with gelatin. Biotinylation of the MSC surface is a critical first step in the gelatin coating process, and in this study, we evaluated the use of biotinylated cholesterol lipid insertion" anchors as a substitute for the covalent NHS-biotin anchors to the cell surface. Streptavidin-eosin molecules where eosin is our photoinitiator can then be bound to the cell surface through biotin-streptavidin affinity. The use of cholesterol anchors increased streptavidin density on the surface of MSCs further driving polymerization and allowing for an increased fraction of MSCs coated with gelatin (83{\%}) when compared to NHS-biotin (52{\%}). Additionally the cholesterol anchors increased the uniformity of the coating on the MSC surface and supported greater numbers of coated MSCs even when the streptavidin density was slightly lower than that of an NHS-biotin anchoring strategy. Critically this improvement in gelatin coating efficiency did not impact cytokine secretion and other critical MSC functions. Proper selection of the cholesterol anchor and the biotinylation conditions supports cellular function and densities of streptavidin on the MSC surface of up to {\~{}}105 streptavidin molecules/$\mu$m2 . In all these cholesterol anchors offer an effective path towards the formation of conformal coatings on the majority of MSCs to improve the retention of MSCs in the heart following AMI."
更多信息
| Species | Mouse |
|---|
相关产品
-
MesenCult™成骨刺激试剂盒（小鼠）小鼠间充质干细胞和胚胎成纤维细胞分化成成骨细胞的完全培养基
-
缺氧培养箱培养室为组织培养提供缺氧环境
-
D-PBS（不含ca++和mg++）Dulbecco的磷酸盐缓冲盐水，不含钙和镁
-
Falcon®锥形管，50 mL用于细胞分离和细胞培养的无菌聚丙烯锥形管
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT STEMCELL, REFER TO WWW.STEMCELL.COM/COMPLIANCE.
