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Cortical Bone Stem Cells Are Beneficial in Recovery After Heart Attack

Cortical bone stem cells (CBSCs) were shown to alter cell death after cardiac reperfusion injury, suggesting a mechanism by which these cells could help patients after myocardial infarction (heart attack).

ABSTRACT

Cortical bone derived stem-cell therapy reduces apoptosis after myocardial infarction.

Am J Physiol Heart Circ Physiol. 2019 Aug 23. doi: 10.1152/ajpheart.00144.2019. [Epub ahead of print]

Hobby AR1, Sharp Iii TE2, Berretta RM3, Borghetti G1, Feldsott E1, Mohsin S1, Houser SR1.

Author information

  1. Physiology, Temple University School of Medicine, United States.
  2. Cardiovascular Center of Excellence, Louisiana State University Health Science Center, United States.
  3. Cardiovascular Research Center, Temple University School of Medicine, United States.

Summary

To comparatively evaluate changes in proliferation and mineralization abilities of dental pulp stem cells (DPSCs) from juvenile and adult rats in a lipopolysaccharide (LPS)-induced inflammatory microenvironment to provide a theoretical basis for the age-related differences observed in DPSCs in repair of inflammatory injury.

Methodology

DPSCs were isolated from juvenile rats (JDPSCs) and adult rats (ADPSCs), and senescence associated β-galactosidase staining was used to compare senescence between JDPSCs and ADPSCs. Effects of LPS on JDPSCs and ADPSCs proliferation were investigated by cell counting kit-8 assays and flow cytometry. Alizarin red staining, quantitative reverse transcription polymerase chain reaction, and western blot assay were used to examine the effects of LPS on mineralization-related genes and proteins in JDPSCs and ADPSCs. Immunohistochemistry was used to compare interleukin-1β (IL-1β) and osteocalcin (OCN) expression in the pulpitis model. Unpaired Student’s t-test and one-way ANOVA were used in statistical analysis.

Results

DPSCs could be isolated from juvenile and adult rat dental pulp tissues. At low concentrations (0.1-1 μg/mL), LPS significantly promoted the proliferation of JDPSCs (P < 0.01) and ADPSCs (P < 0.01 or P < 0.05), with the effect being stronger in JDPSCs than in ADPSCs. In addition, mineralized nodules and the expression of mineralization-related genes (OCN, DSPP, ALP, BSP) increased significantly after stimulation with LPS (0.5 μg/mL) in JDPSCs and ADPSCs (P < 0.01 or P < 0.05), and JDPSCs displayed a more obvious increase than did ADPSCs. Western blots revealed OCN and ALP expression levels in JDPSCs treated with LPS were significantly upregulated (P < 0.05); meanwhile, ALP expression in ADPSCs increased slightly but significantly (P < 0.05), and OCN expression was not affected. Finally, IL-1β expression was significantly higher (P < 0.05) and OCN expression was significantly lower (P < 0.05) in the inflamed dental pulp of adult rats than in juvenile rats.

Conclusions

A certain degree of inflammatory stimulation promoted the proliferation and mineralization of DPSCs; however, this effect declined with age. The DPSCs of older donors in an inflammatory microenvironment have a weaker repair ability than that of young donors, who are better candidates for tissues damage repair.