Tissue Development, Repair, and Remodeling - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 670

Chapter 11
Tissue Development, Repair, and Remodeling
Tissue growth as well as repair of tissue injury is controlled by many regulators
such as growth factors that both reorganize the cytoskeleton and cell adhesions and
trigger the action of transcription factors, thereby enabling proper cell migration and
lodging as well as adaptation to environmental conditions. Cell wall extensibility
and junctional communications are involved in tissue growth. In adults, cell
differentiation happens during normal cell turnover as well as during tissue repair.
Tissue remodeling caused by a sustained, time-dependent mechanical stress field
and chemical cues, possibly associated with angiogenesis, rely on the coordination
between regulated cell proliferation, differentiation, migration, and apoptosis to
determine the correct tissue configuration [ 1376 ].
Repair, or healing, involves a series of rapid infiltrations and accumulations of
various cell populations that deposit a new matrix and mature (Table 11.1 ). Once
they have completed their tasks, some involved cell types are eliminated prior to
the progression to the next phase of healing via apoptosis (Vol. 2 - Chap. 4. Cell
Survival and Death). Apoptosis allows elimination of entire cell populations without
tissue damage or inflammation.
During the proliferation phase of tissue repair, collagen-3 prevails. During the
maturation, collagen-3 is gradually degraded and collagen-1 produced. Moreover,
collagen fibers that are originally disorganized rearrange, crosslink, and align along
tension lines [ 1377 ]. Blood vessel density decays as local activity attenuates. Some
blood vessels are removed by apoptosis.
When cells undergo apoptosis, tiny regions of the plasma membrane pinch
off and form vesicles, the so-called apoptotic bodies , that are shed and carry
messages from dying cells to healthy ones to promote repair. Apoptotic bodies from
dying endothelial cells that are taken up by healthy endothelial cells heightens the
expression of the Cxcl12 gene [ 1378 ]. Chemokine CXCL12 counteracts apoptosis
and recruits progenitor cells for repair. In apoptotic bodies, microRNA-126 prevents
the synthesis of an inhibitor of CXCR4, the CXCL12 receptor. This GPCR then
triggers a feedback loop that augments the production of CXCL12 to attract
progenitor cells for new tissue generation.