February 7, 2007
Embryology Biology 441 Spring 2007 Albert Harris
Embryonic artery, wrapped in collagen fibers (yellow)
Finish Mesoderm, and then EndodermFirst sub-topic, blood vessels: which are formed from mesoderm.
Capillaries; Veins; Arteries; + also Lymphatic ducts.
In all of these, the innermost lining is a sheet of a special kind of epithelial cell, called "endothelial cells" "endothelium"
(Don't be fooled by the name, these are NOT formed by endoderm!)
Capillaries are narrow hollow tubes of endothelial cells, with little or no other reinforcement. Despite their very thin walls, the pressure in capillaries is more than in veins, and in many capillaries the pressure is almost as strong as in arteries!!?
But earlier in the course you learned about P = C*T + c*t
Veins are much wider tubes, in which the inner-most lining is a tube of endothelial cells, but they are surrounded by many layers of fibroblasts (mesenchymal cells), and wrapped by Type I collagen fibers (which are mostly secreted by the fibroblasts).
Arteries: innermost layer of endothelial cells
Elastin is rubber-like, 'stretchy'; In contrast to collagen which forms strong nylon-like fibers and sheets.
The aorta differs from other arteries in that its walls have many fewer smooth muscle cells, and many more fibroblasts, and LOTs more elastin, along with the collagen fibers.
Here is a photograph I took of a cross section through a vein and an artery. (a normal artery)
The artery is in the upper-middle.
One of the biggest causes of human death and disability is the disease "atherosclerosis". It is true that if the concentration of cholesterol in your blood is high, then you are more likely to have your arteries blocked by atherosclerotic "plaque".
A cross section of a human artery blocked by atherosclerosis.
It is definitely NOT true that cholesterol sticks to the inside of anyone's arteries. Clotted blood & blood platelets do stick there.
Why does nearly everyone tell you that cholesterol sticks inside your arteries? I don't know why! It's just an Aesop's fable!
WHAT IS THE TRUE STORY:
* Among all those extra smooth muscle cells, that are bulging into the space where the blood should flow, cholesterol does accumulate. So there is some kind of connection.
But many of you will be going into medicine or medical research, so you should be told the truth, not Aesop's fables, and in this case the truth is that nobody really understands what's happening.
One theory: The blockages are tumors of the smooth muscle cells, analogous to many small cancers, caused by somatic mutations.
Another theory: Turbulence in the blood stimulates blood platelets to secrete PDGF (Platelet-Derived Growth Factor), a protein which is known to stimulate smooth muscle cells to grow and divide and also is a chemotactic attractant for them.
Notice that neither of these theories predicts the (true) fact that these over-growths of smooth muscle cells are larger and worse in animals and people who have more cholesterol in their blood.
If you could invent some possible reasons, and also how to test them, then that would be a HUGE contribution to medical science.
Research science is full of riddles and paradoxes of this kind.
Usually you can't just observe complex phenomena.
Inventing theories tells you what details to be curious about!
Please invent as many possibilities as you can, and send or email them to me, and I will make a long list of every explanation any of us can think of. (but NOT on the exams)
The following are entirely imaginary; there is no evidence for them. (yet)
2) Cholesterol deposits make smooth muscle cells more sensitive to PDGF.
3) Cholesterol stimulates platelets to secrete more PDGF, and it's just a coincidence that cholesterol also gets deposited in among the extra smooth muscle cells.
4) Cholesterol deposits prevents apoptosis of extra smooth muscle cells, so that excess accumulations of smooth muscle are not eliminated..
5) Cholesterol somehow causes or allows smooth muscle cells to pull more strongly on collagen fibers, or elastin fibers, or to contract more strongly.
6) Cholesterol deposits between smooth muscle somehow stimulates them to divide.
10) please invent more theories!!!
Most of these are in the yolk sac, in birds and mammals.
Maybe that's why mammal embryos continue to have yolk sacs?
Red blood cells and white blood cells differentiate inside;
The yolk sac is one of several different organs that are used as locations for the hemopoietic stem cells which form red blood cells (and also white blood cells). These stem cells move to the liver, and later to the bone marrow.
Embryonic and fetal hemoglobins are different from (and coded for by different genes than) the hemoglobin we have in the red blood cells we make after birth. Fetal hemoglobin binds oxygen slightly more strongly than adult hemoglobin, which increases the amount of oxygen that is transferred across the placenta from the blood of a pregnant woman to the blood of the fetus developing inside her. Two other interesting aspects are:
#1) The genes for embryonic and fetal hemoglobin proteins are directly adjacent to the genes for adult hemoglobins, with the early blood cells activating one gene, and then later blood cells activating the gene next to that one. The mechanism isn't known, nor whether there is any similarity to the mechanisms that cause adjacent Hox genes to be transcribed in adjacent tissues.
#2) A few people continue to make fetal hemoglobin all their life, instead of switching to the adult hemoglobin genes, and the symptoms of this are almost unnoticeable! So far as I know, it hasn't yet been discovered what mechanism causes this; but it could become a new and better treatment for sickle-cell anemia (and other genetic defects of adult hemoglobins), if you could discover a drug or other treatment that switches their hemopoietic stem cells back to transcribing the genes for fetal hemoglobin.
The Skeleton: formed by mesodermal cells,
except the face, where skeleton is neural crest cells
Vertebrate skeletons are made partly of bone and partly cartilage.
Bone compared with Cartilage
Bone is stronger and more rigid,
Cartilage is lighter, flexible, weaker,
Bone is a tightly woven composite of 1/3 type I collagen fibers,
embedded among crystals of calcium phosphate (2/3rds by weight)
(& also fluoride and hydroxide) (dentine is almost the same)
Bone is made (but not really secreted!) by osteocytes. (= osteoblasts)
Deposition of bone is called "ossification".
Another special differentiated cell type (osteoclasts) constantly dissolves and destroys bones. Bone is a very dynamic tissue, being constantly
destroyed and remade. When osteocytes don't keep up with the osteoclasts
the result is osteoporosis. There are many unsolved problems here.
Cartilage is a mixture of type II collagen and chains of sugar molecules that have sulfate groups covalently bound to them. The sulfates ionize,
and their negative charges keep a cloud of cations (like Na+) nearby.
Cartilages grow partly by increased synthesis of sulfated sugars, and partly by selective cutting of both the internal and surface collagen.
As an analogy, imagine controlling the shape of a balloon partly by forming more gas inside, and partly by weakening the rubber.
|Elastic cartilage of ear||Elastic cartilage seen by polarization microscopy|
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