Telomere Length Reprogramming in Embryos and Stem Cells

Kalmbach, Keri; Robinson, L.G.; Wang, Fang; Liu, Lin; Keefe, David L.

doi:10.1155/2014/925121

Cited by 41 publications

(33 citation statements)

References 70 publications

(70 reference statements)

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“…However, the ALT and telomerase pathways may coexist during reprogramming of induced pluripotent stem cells (146). Moreover, in embryonic stem cells, the ALT-related proteins, α-thalassemia mental retardation X-linked and the histone-H3 variant (H3.3), colocalize with telomeres within the promyelocitic leukemia (PML) bodies (63,157,232). The crucial function that PML has in cancer progression has led to the discovery of the important role that ALT has in cancer stem cells (42,71,359).…”

Section: Identification Of Senescent Cpcsmentioning

confidence: 99%

Aging Effects on Cardiac Progenitor Cell Physiology

Rota

Goichberg

Anversa

et al. 2015

Comprehensive Physiology

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Cardiac aging has been confounded by the concept that the heart is a postmitotic organ characterized by a predetermined number of myocytes, which is established at birth and largely preserved throughout life until death of the organ and organism. Based on this premise, the age of cardiac cells should coincide with that of the organism; at any given time, the heart would be composed of a homogeneous population of myocytes of identical age. The discovery that stem cells reside in the heart and generate cardiac cell lineages has imposed a reconsideration of the mechanisms implicated in the manifestations of the aging myopathy. The progressive alterations of terminally differentiated myocytes, and vascular smooth muscle cells and endothelial cells may represent an epiphenomenon dictated by aging effects on cardiac progenitor cells (CPCs). Changes in the properties of CPCs with time may involve loss of self-renewing capacity, increased symmetric division with formation of daughter committed cells, partial depletion of the primitive pool, biased differentiation to the fibroblast fate, impaired ability to migrate, and forced entry into an irreversible quiescent state. Telomere shortening is a major variable of cellular senescence and organ aging, and support the notion that CPCs with critically shortened or dysfunctional telomeres contribute to myocardial aging and chronic heart failure. These defects constitute the critical variables that define the aging myopathy in humans. Importantly, a compartment of functionally competent human CPCs persists in the decompensated heart pointing to stem cell therapy as a novel form of treatment for the aging myopathy.

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Section: Identification Of Senescent Cpcsmentioning

confidence: 99%

Aging Effects on Cardiac Progenitor Cell Physiology

Rota

Goichberg

Anversa

et al. 2015

Comprehensive Physiology

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“…Telomere biology became a field that holds great promise for medicine, particularly for aging and age-related diseases, including diabetes mellitus, cardiovascular diseases, liver disorders and cancer, and their status in stem cells as compartments which contribute to tissue homeostasis obtained particular attention [8] .…”

Section: Research Highlightmentioning

confidence: 99%

Correlation between telomere maintenance and stemness of mesenchymal stem/stromal cells

Trivanović

Krstić

Jauković

et al. 2016

Telomere Telomerase

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“…As such, human (h)ESCs are capable of being passaged over 120 times with no decrease in telomerase activity, telomere length and pluripotency potential. 18 Several recent reviews [19][20][21] have highlighted different mechanisms by which telomeres and TERT are affected by pluripotency. These discussions tend to be singularly focused with pluripotency acting as an effector.…”

Section: Introductionmentioning

confidence: 99%

The role of telomeres and telomerase reverse transcriptase isoforms in pluripotency induction and maintenance

2016

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Telomeres are linear guanine-rich DNA structures at the ends of chromosomes. The length of telomeric DNA is actively regulated by a number of mechanisms in highly proliferative cells such as germ cells, cancer cells, and pluripotent stem cells. Telomeric DNA is synthesized by way of the ribonucleoprotein called telomerase containing a reverse transcriptase (TERT) subunit and RNA component (TERC). TERT is highly conserved across species and ubiquitously present in their respective pluripotent cells. Recent studies have uncovered intricate associations between telomeres and the self-renewal and differentiation properties of pluripotent stem cells. Interestingly, the past decade's work indicates that the TERT subunit also has the capacity to modulate mitochondrial function, to remodel chromatin structure, and to participate in key signaling pathways such as the Wnt/b-catenin pathway. Many of these non-canonical functions do not require TERT's catalytic activity, which hints at possible functions for the extensive number of alternatively spliced TERT isoforms that are highly expressed in pluripotent stem cells. In this review, some of the established and potential routes of pluripotency induction and maintenance are highlighted from the perspectives of telomere maintenance, known TERT isoform functions and their complex regulation.

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Telomere Length Reprogramming in Embryos and Stem Cells

Cited by 41 publications

References 70 publications

Aging Effects on Cardiac Progenitor Cell Physiology

Aging Effects on Cardiac Progenitor Cell Physiology

Correlation between telomere maintenance and stemness of mesenchymal stem/stromal cells

The role of telomeres and telomerase reverse transcriptase isoforms in pluripotency induction and maintenance

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