Mouse Galactosidase, Beta ELISA Kit (DEIA-BJ2470)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
Serum, plasma, cell culture supernatants, body fluid and tissue homogenate
Species Reactivity
Mouse
Intended Use
Mouse Galactosidase, Beta ELISA Kit kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of the Galactosidase, Beta. This ELISA kit is for research use only, not for therapeutic or diagnostic applications.
Contents of Kit
1. MICROTITER PLATE: 96 wells
2. ENZYME CONJUGATE: 6.0 mL or 10 ml
3. STANDARD A-F: 1 vial each
4. SUBSTRATE A: 6 mL
5. SUBSTRATE B: 6 mL
6. STOP SOLUTION: 6 mL
7. WASH SOLUTION (100 x): 10 mL
8. BALANCE SOLUTION: 3 mL
Storage
All components of this kit are stable at 2-8°C until the kit's expiration date.
Detection Range
5-100 μ/L
Sensitivity
1.0μ/L

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References


Augmentation of Bone Regeneration by Depletion of Stress-Induced Senescent Cells Using Catechin and Senolytics

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES

Authors: Honda, Yoshitomo; Huang, Anqi; Tanaka, Tomonari; Han, Xiaoyu; Gao, Beiyuan; Liu, Haitao; Wang, Xinchen; Zhao, Jianxin; Hashimoto, Yoshiya; Yamamoto, Kazuyo; Matsumoto, Naoyuki; Baba, Shunsuke; Umeda, Makoto

Despite advances in bone regenerative medicine, the relationship between stress-induced premature senescence (SIPS) in cells and bone regeneration remains largely unknown. Herein, we demonstrated that the implantation of a lipopolysaccharide (LPS) sustained-release gelatin sponge (LS-G) increases the number of SIPS cells and that the elimination of these cells promotes bone formation in critical-sized bone defects in the rat calvaria. Histological (hematoxylin-eosin and SA-beta-gal) and immunohistological (p16 and p21 for analyzing cellular senescence and 4-HNE for oxidation) staining was used to identify SIPS cells and elucidate the underlying mechanism. Bone formation in defects were analyzed using microcomputed tomography, one and four weeks after surgery. Parallel to LS-G implantation, local epigallocatechin gallate (EGCG) administration, and systemic senolytic (dasatinib and quercetin: D+Q) administration were used to eliminate SIPS cells. After LS-G implantation, SA-beta-gal-, p16-, and p21-positive cells (SIPS cells) accumulated in the defects. However, treatment with LS-G+EGCG and LS-G+D+Q resulted in lower numbers of SIPS cells than that with LS-G in the defects, resulting in an augmentation of newly formed bone. We demonstrated that SIPS cells induced by sustained stimulation by LPS may play a deleterious role in bone formation. Controlling these cell numbers is a promising strategy to increase bone regeneration.

iPSC-Derived MSCs Versus Originating Jaw Periosteal Cells: Comparison of Resulting Phenotype and Stem Cell Potential

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES

Authors: Umrath, Felix; Weber, Marbod; Reinert, Siegmar; Wendel, Hans-Peter; Avci-Adali, Meltem; Alexander, Dorothea

Induced pluripotent stem cell-derived mesenchymal stem cell-like cells (iMSCs) are considered to be a promising source of progenitor cells for approaches in the field of bone regeneration. In a previous study, we described the generation of footprint-free induced pluripotent stem cells (iPSCs) from human jaw periosteal cells (JPCs) by transfection of a self-replicating RNA (srRNA) and subsequent differentiation into functional osteogenic progenitor cells. In order to facilitate the prospective transfer into clinical practice, xeno-free reprogramming and differentiation methods were established. In this study, we compared the properties and stem cell potential of the iMSCs produced from JPC-derived iPSCs with the parental primary JPCs they were generated from. Our results demonstrated, on the one hand, a comparable differentiation potential of iMSCs and JPCs. Additionally, iMSCs showed significantly longer telomere lengths compared to JPCs indicating rejuvenation of the cells during reprogramming. On the other hand, proliferation, mitochondrial activity, and senescence-associated beta-galactosidase (SA-beta-gal) activity indicated early senescence of iMSCs. These data demonstrate the requirement of further optimization strategies to improve mesenchymal development of JPC-derived iPSCs in order to take advantage of the best features of reprogrammed and rejuvenated cells.

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