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Cell Science, Stem Cell Research &
Pharmacological Regenerative Medicine
November 29-30, 2017 | Atlanta, USA
Annual Congress on
Adv cel sci tissue cul 2017 | Volume 1 Issue 2
An attempt will be made to provide a short conceptual
review to integrate, from an evolutionary perspective,
how the emergence of gap junctional intercellular
communication helped to bring about multi-cellularity
and new adaptive phenotypes. This new fundamental
biological function of the metazoans was needed to provide
homeostatic control of newcellular functions of an interacting
society of different cell types existing in a 3-dimensionalunit.
Changing paleo-physics- and -chemistry of the earth led to
single celled organisms that metabolized sugar via glycolysis
and survived via symmetrical cell division and occasional
mutations. With the appearance of oxygen-producing
phytoplankton, the single cell organism, the mitochondrion,
symbiotically- fused with a primitive cell to form the first
multi-cellular organism, which could metabolize glucose via
oxidative phosphorylation. The new society of adherent cells
developed new strategies for adaptive survival. New genes
and phenotypes included: growth control, differentiation,
programmed cell death; senescence; regulation of gene
expression-“epigenesis”; germline and somatic stem cells;
asymmetrical cell division; and anoxic stem cell niches. The
evolutionary development of the normal human organism,
starting from a single “toti-potent” stem cell to the mature,
reproductive and self-aware being, consisting of over 100
trillion cells, of which 200 different cell types and having
three major functional cells- (organ-specific stem cells;
their progenitor derivative cells; and their differentiated
daughters), could only come about by a delicate homeostatic
integrated feedback system of extra-, intra- and gap
junctional inter-cellular communication (GJIC). Since GJIC
occurs in all organs, any disruption of the three forms of
cell communication mechanisms by genetic or epigenetic
factors, particularly during embryonic, fetal and neonatal
periods, could lead to alteration of risks to diseases later in
life (i.e., the Barker hypothesis). Chronic disruption of these
signaling mechanisms in the adult organs could also lead to
several kinds of chronic, stem cell-based diseases, diabetes,
cancer, atherogenesis and premature aging.
e:
A conceptual integration of extra-, intra- and gap junctional-intercellular communication in the evolution
of multi-cellularity and stem cells: How disrupted cell-cell communication during development can affect
diseases later in life?
James E Trosko
Michigan State University, USA