BMED 2801 – Lecture 7 – Histology: Cells and Tissues
CELL RENEWAL
Static populations of cells – cells that rarely/never divide.
• Central nervous system cells once mature NEVER divide – no mitotic activity
• Skeletal & cardiac muscle cells RARELY divide (in the case of steroid intake/exercise for skeletal
muscle bulk  increasing indv. cell size, not the number of cells)
Stable populations:
- physical, chemical damage  response = increase in mitotic activity
- Mitotic activity is stimulated in the basal cells/stem cells – cell damage at the apical surface of
epithelium initiates mitotic activity to renew epithelial tissue.
- e.g. smooth muscle, endothelium, epithelium, fibroblast, and perichondrial cells (the fibrous
membrane that covers the surface of cartilage except at joints)
• Cell division occurs in mature cells on a NEEDS basis
• maintains a stable cell population
Renewing cell populations
• Regular mitotic activity
• Slowly or rapidly renewing
Mitotic activity rates vary
Chemotherapy – designed to target rapidly dividing cells (the tumour), but normal rapidly diving
cells are also slowed = hair loss, ulcers, GIT problems (enteriocytes can not replenish quick
enough to maintain epithelial integrity), thinning of skin, slow blood cell turnover.
Necrosis Vs Apoptosis
Necrosis:
The damage and death of cells in a tissue or organ caused by disease or injury e.g. decreased blood
supply= gangrene. Leads to an Inflammatory reaction plasma membrane is disrupted (toxins punch
holes on membrane, dysfunction of channels or receptors on membrane etc) = changes in osmotic
gradient  causing swelling of the cell = cell death.
Problem: during necrotic cell death what is in the cells enters extracellular space e.g. lysosomal enzymes
= causing inflammation.
Apoptosis:
A form of cell death necessary to make way for new cells and to remove cells who’s DNA has been
damaged, loss to the point at which cancerous change is liable to occur
Programmed cell death, normal process - preventing accumulation disorders.
As cells functional ability deteriorates a genetic or humeral response is generated – causing breakdown
of the nucleus, fragmentation of DNA, loss in cell volume - but plasma membrane remains in tack  an
apoptotic body is formed - a membrane bound bundles containing non-functional organelles – these will
be engulfed by macrophages or reused.
CELL POLARITY
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Genetically controlled cell arrangement – is cell polarity
Correct cell polarity is important for the proper functioning of a cell
Lateral plasma membrane (Between cells)
Barrier between lumen and underlying tissue
(The basal plasma membrane – rest on a connective tissue/basement membrane with an epithelium)
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e.g. In Gut – something needs to be absorbed in the columnar epithelial cell of large
intestine
need the apical domain up – with certain receptor or microvilli to increase surface area
Also, need to hold these cells together and keep the integrity of the tissue so leakage does
not occur – causing inflammation and damage to the underlying tissue.
THE BASAL PLASMA MEMBRANE
3 distinct features:
• Plasma membrane infoldings increase surface area = stronger type of connection
• Cell-to-extracellular matrix junctions anchor cell – hold epithelial cell to underlying basement membrane
– hemidesmosomes.
• Basement membrane – produced by underlying connective tissues cells and epithelial cells.
Plasma membrane infoldings
Nucleus
Infolding of basal plasma membrane – railway tracks running
up/down. – This increases SA – helps anchor plasma
membrane to connective tissue and basement membrane.
High density of mitochondria in this region because - a lot of
transport between basal surface to underlying tissue.
E.g. striated ducts in Kidney
Mitochondria associated with them
Active transport + energy
Cell-to-extracellular matrix junctions
Maintain morphological integrity of cell-CT
(1) Focal adhesions
Actin filaments into basement membrane
(2) Hemidesmosomes (half a desmisome)
Intermediate filaments into basement membrane
Within cytoplasm of cell filaments hold protein plaque in
place.
Plasma membrane
Anchoring proteins – embed
plasma membrane down into
underlying collagen of
basement membrane.
Hemidesmosomes anchoring junction -holds epithelium
down.
BASEMENT MEMBRANE
How do we see it LM?
Haematoxylin + eosin  PINK
Periodic Acid Shift – will pick up the proteoglycans to stain MAGENTA
Silver reduction will pick up the collagen fibres to stain  BLACK (show connective tissue- underneath
epithelium)
Where is it located?
Between epithelial cells & connective tissue (basal border)
Surrounds PNS support cells, adipocytes & muscle cells
What does it do?
(1) Attachment of epithelial cells to underlying connective tissue
(2) Influence differentiation & proliferation of epithelial cells from stem cells
E.g. asthmatics – inflamed airways- loose psudostratified columnar epithelium  cause basement
membrane to be exposed- cause BM to stimulate stem cells to undergo mitosis to replace above
epithelium & BM to increase in thickness.
- Via Scaffolding
cell loss/damage but Basement Membrane remains
guides cell growth during regeneration
- Via Polarity induction
(3) Compartmentalization – separates CT from functional epithelium, muscle and nerve tissue  allowing
for communication and individual functioning.
(4) Filtration - Via ionic charges across the BM and integral spaces within the BM  ionic filter – creates
osmotic gradient across, helps filter things between connective tissue, epithelium and vice/versa.
The thickness of basement membrane – will reflect the condition of the overlying epithelium.
What does it look like with the EM?
Thick basement membrane –
asthma, infections,
pneumonia etc. cause
epithelia to be exposed, BM
tries to protect underlying
tissue and builds up. The
thickness of BM, reflects the
chronicity of the events
occurring in the above cells.
Eletron microscope
Basal lamina (the basement membrane is called the basal lamina when viewed with the EM)
• Structural attachment site
• 40nm – 60nm wide
Type IV collagen fibrils (lots of collagen fibrils =collagen fibre) anchor to epithelial cell
Proteoglycans  regulate ion passage
Laminin  anchor to epithelial cell
Fibronectin & entactin  anchor to CT
Lamina lucida
40nm wide
Integrins = fibronectin receptors  anchor
Reticular lamina
Reticular fibres (type III collagen)
Produced by CT