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Articles by J. Johnson
Total Records ( 2 ) for J. Johnson
  M.E. Boroujeni , P. Gowda , J. Johnson , J. Rao and S. Saremy
  Bone marrow derived-Human Mesenchymal stem cells (hMSCs) are non-hematopoetic, stromal cells that demonstrate multilineage differentiation capacity and being capable to give rise to diverse tissues, including bone and cartilage. Due to this capability, hMSCs are currently evaluated for regenerative medicine, repopulating injured tissues and clinically ablated diseased tissues with healthy, terminally differentiated cells. Thus, for therapeutic applications, enough numbers of homogenous MSCs are required. In this study, the population doubling of bone marrow derived hMSCs was assessed in early and late passages. It was noted that in healthy cells, generally, the population doubling increases over time due to the slower rate of cell growth. Subsequently, the mesengenic multipotency of BM-MSCs for chondrogenesis, osteogenesis and adipogenesis was investigated in early and late doublings. According to our findings, the early passage hMSCs treated with the differentiation agents exhibited approximately 100, 48±10.33 and 28.6±6.62% osteocytes, chondrocytes and adipocytes, respectively. Whereas, the late passage hMSCs subjected to the differentiation agents only demonstrated the high degree of osteogenicity but they revealed neither chondrogenicity nor adipogenicity. Furthermore, the Expression of Oct4, Sox2 and Nanog genes in undifferentiated human BM-derived MSCs was studied. The result revealed the Oct4 is expressed at very low levels in early passage MSCs and disappeared at late passage however Nanog and Sox2 were almost undetected in MSCs. In conclusion, the proliferation rates and other properties of the cells gradually change during expansion and therefore, it is recommended to not expand hMSCs beyond four or five passages.
  T. C Thomson , K. E Fitzpatrick and J. Johnson
 

A great deal of evolutionary conservation has been found in the control of oocyte development, from invertebrates to women. However, little is known of mechanisms that control oocyte loss over time. Oocyte loss is often assumed to be a result of oocyte-intrinsic deficiencies or damage. In fruit flies, starvation results in halted oocyte production by germline stem cells and induces oocyte loss midway through development. When we fed wild-type flies the bacterial compound Rapamycin (RAP) to mimic starvation, production of new oocytes continued, but mid-stage loss sterilized the animals. Surprisingly, follicle cell invasion and phagocytosis of the oocyte preceded any signs of germ cell death. RAP-induced egg chamber loss was prevented when RAP receptor FKBP12 was knocked down specifically in follicle cells. Oogenesis continued past the mid-stages, and these mutants continued to lay embryos that could develop into normal adults. Hence, intact healthy oocytes can be destroyed by somatic cells responding to extrinsic stimuli. We termed this process inducible somatic oocyte destruction. RAP treatment of mouse follicles in vitro resulted in phagocytic uptake of the oocyte by granulosa cells as seen in flies. We hypothesize that extrinsic modes of oocyte loss occur in mammals.

 
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