Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
56 Cards in this Set
- Front
- Back
|
What primary AA components are in the collagen subunit? What are their purposes?
|
Glycine present at every THIRD amino acids: produces a linear peptide
Also rich in proline and hydroxyproline: stabilize the helical structure |
|
|
What is meant by triple helical domain?
|
Three linear peptides assemble to form
"collagenous domain" of collagen |
|
|
Where are all collagen synthesized with? What must happen to produce fibrils? Collagen is synthesized as individual chains called what?
|
Non-collagenous domains
Non-collagenous portions must be removed Individual chains called PROCOLLAGEN |
|
|
What do procollagen chains contain that allow them to assemble into a triple helical molecule? Where does this occur?
|
Registration peptides:present within the noncollagenous domains, they will then wind up into this triple helical molecule
Occurs within the cell |
|
|
What happens after procollagen is formed? What is the new product called, and is it soluble or insoluble?
|
Excreted out to the cell, where procollagen peptidases cleave the nonhelical registration peptides, transforming procollagen into INSOLUABLE tropocollagen
|
|
|
Because tropocollagen is relatively insoluable, what will happen? What does it form? Are there noncollagenous or collagenous domains present (or both)?
|
Aggregate to form collagen fibrils, and they are covalently crosslinked to form fibrilar structure
Only collagenous domains remain |
|
|
What happens after collagen fibrils are formed?
|
Associate to form collagen FIBERS (assembly of colagen fibrils)
|
|
|
Are fibroblasts transient or resident?
|
Resident
|
|
|
What are the four main collagen types?
|
Collagen 1, 2, 3, 4 difficult I know
|
|
|
Which collagen fiber is most abundant? Where is it found most abundant?
|
Collagen 1: found almost everywhere: GREATEST ABUNDANCE is in the SKIN AND BONE (ubiquitous)
|
|
|
Collagen 2 forms fibrils or fibers? How about collagen 1? Where is collagen 2 found?
|
Collagen 2 forms fibrils, collagen 1 forms fibers; collagen 2 is found in cartilage, MOST ABUNDANT in hyaline and elastic cartilage
|
|
|
Collagen 3: fibers or fibrils? What kind? What is one place it is found?
|
Fibers (very different from collage 1) very difficult to see these types unless with special stains
Fibers are called Reticular Fibers i.e. lamina reticularis |
|
|
Collagen IV: fibers or fibrils? Forms what? why?
|
Does not form EITHER-they form NETWORKS
because noncollagenous domains are not cleaved off |
|
|
Skin is what kind of tissue? what type of collagen is found there?
|
Skin is DENSE
IRREGULAR CONNECTIVE tissue Type 1 collagen is found (all wavy and weird) |
|
|
Tendons are what kind of tissue? what type of collagen is found there?
|
DENSE
REGULAR CONNECTIVE tissue Type 1 collagen primarily (has little blue cigar shpaes in lines almost--fibroblasts) |
|
|
What is the different between loose and dense connective tissue?
|
How much type 1 collagen is there, and where you're looking at
loose: functions to support |
|
|
Epithelial linings of GI, GU and respiratory tracts have what kind of tissue? What is the nickname? What type of collagen? What is the ground substance? What's another tissue that functions in packing
|
Loose connective tissue
spacey aka "PACKING" tissue ground substance: proteoglycan loose: functions to support tubes packing: adipose tissue (also connective) |
|
|
Reticular fibers are what kind of collagen? Can they been seen by H&E? Where can they be found? What do they look like?
|
Type 3 (stick like)
Nope (special stain, like silver) Found in highly cellular organs such as spleen and liver::form a SUPPORTING FRAMEWORK Thin and dainty, but they're still fibers |
|
|
What does elastic fiber do? What kind of linking is present? Where are they present?
|
Adds elasticity to tissue::can stretch and relax
Cross linking between elastin molecules They're present everywhere, but they're abundant in a couple of diff tissues |
|
|
What are elastic fibers composed of? What are they similar to? Where are they assembled?
|
similar to collagen
Tropoelastin, fibrilin I and II, and MAGP (microfibril associated glycoprotein) Like collagen, assembled in the EXTRACELLULAR ENVIRONMETN |
|
|
What is elastin fibers primarly synthesized by?
|
Fibroblasts, or fibroblast equivalents, or smooth muscle cells
|
|
|
How are elastic fibers first formed--what is it called after it is secreted out to the EC space? How are these compared to collagen?
|
It is FIRST PROELASTIN in the cell, which is secreted out to the EC, which it becomes TROPOELASTIN (like procollagen and then tropocollagen)
|
|
|
What else does the cell synthesize besides proelastin? Where are they found? When do these partake in the elastin fiber formation? What is this called? How is this similar to collagen?
|
Fibrillin I and II and MAGP
Are also secreted out from the cell These assemble outside together WITH the tropoelastin to form IMMATURE ELASTIC FIBERS (the collagen fibrils for collagen) |
|
|
What happens after formation of immature elastic fibers? How is this similar to collagen?
|
They are bundled together to become mature elastic fibers (like collagen fibers)
|
|
|
How are elastic fibers presented in supporting tissues? Which is found in large walls of blood vessels like the aorta?
|
Either as fibers or as sheets
Walls of large blood vessels: SHEETS |
|
|
In Marlan syndrome, what is deficient, and what does this result in? Why do these patients die early?
|
Deficient in fibrillin 1::results in lack of elastin fiber formation
Die from mitral valve prolaspe and aortic dissection:: The large blood vessels are abundant in elastin fibers/sheets, like how the aorta has elastin sheets::absence results in split of walls of aorta, and blood goes into the wall, and where the mitral valve should be sealed, it expands with no elasticity to control it and doesn't close properly |
|
|
How can extracellular matrix proteins be degraded (a class of enzymes)? Why? What are they involved with (list some examples)?
|
Cells must be able to modify its immediate surrounds, which includes degrading extracellular matrix proteins (so it's not a bad thing...)
Matrix metalloproteinases (MMPs) because of their dependenc on metal ions for catalytic activity, and their potent ability to degrade structural proteins of the ECM NOTE: can also include cells that move in and out of ECM or the epithelial cells It's called MMP's because of their dependence on METAL ions Can be involved in embryonic deveopment, tissue morphogenesis, wound repair, inflammatory diseases, cancer |
|
|
Do MMPs need to be regulated? In what state are they synthesized? What is this called? What is done with this to work?
|
Because they're so potent, they MUST be regulated, and at multiple levels. They are made in an inactive form : pro-MMP
They are activated and can be protelytically processed and inactivated |
|
|
Once activated, what is the protein inhibitor called that can inhibit the MMPs?
|
Bound by protein inhibitor collectively known as TIMPS (tissue inhibitors of metalloproteases)
|
|
|
Are MMPs always expressed?
|
Cells involved with synthesizing MMPs almost ALWAYS expresses them (not necessarily true in disease, however)
|
|
|
How are MMPs localized to the ECM? When can it be destroyed?
|
Can be bound by extracellular molecules and localized there, OR
it can bind to a receptor on the cell surface and bind there At this point, it can also be endocytosed and destroyed |
|
|
What are the 6 ways MMPs can be regulated?
|
Proteolytic activation,
Proteolytic processing and inactivation Protein inhibition (TIMPs) ECM localization Cell surface localization Endocytosis and intracellular degradation |
|
|
How are MMps involved with diseases such as cancer? What is overexpressed?
|
Invading tumor cells express activated MMPs allow degradation of basement membrane components and structureal proteins in the underlying connective tissue?
Tumor cells overexpress integrins, allow for facilitating progression in the connective tissue and get into blood and go elsewhere |
|
|
What are the two types of connective tissue cels?
|
Resident cells and transient cells
|
|
|
What are the resident cells?
|
Fibroblasts (or equivalents) and adipocytes
|
|
|
What are the transient cells?
|
Immune system related
Mast cells, macrophages, plasma cells, lymphocytes, eosinophils |
|
|
What do fibroblasts synthesize? What are the fibroblast equivalents in cartilage, bone, and teeth?
|
proteoglycans, collagen, and elastin
Cartilage:CHONDROBLASTS Bone: OsteoBLASTS Teeth: ODONTOBLASTS |
|
|
Where is Type 1 collagen present, and what synthesizes in the respective tissues?
|
Bone, tendon, dentin, skin
FIBROBLASTS: tendon and skin OSTEOBLASTS: bone ODONTOBLASTS: dentin |
|
|
Where is Type 2 collagen present, and what makes it?
|
Hyaline and elastic cartilage, synthesized by chondroblasts
|
|
|
Where is type 3 collagen present, and what makes it?
|
Bone marrow and lymphoid organs (and lamina reticularis =) )
synthesized by FIBROBLASTS called RETICULAR CELLS |
|
|
What is type IV collagen synthesized by?
|
Epithelial cells
|
|
|
What is a mesenchymal cell? What does it make? Where are they found? What does it look like? What else is there?
|
It is an immature FIBROBLAST cell that can differentiate into ANY fibroblast equivalent (chondrocytes, bone cells, fibroblasts itself) AS WELL AS ADIPOCYTES (fat cell) AND smooth muscle cells
Found in embilical card in a consistency called "Wharton's jelly" Has large oval nuclei, and very long cytoplasmic processes, typically found as part of a tissue called teh PRIMITIVE MESENCHYME NO COLLAGEN OR ELASTIC FIBERS::mostly ground substance and cells (no mature fibers) |
|
|
What are mature fibroblasts condensed by? What can you see? How do mature fibroblasts maintain supporting tissues?
|
Condensed by collagen fibers
(slide of dense irregular connective tissue) Usually all you can see is nucleus (cytoplasmic fibers are squeezed) Maintain by continuous turnover of ECM components |
|
|
Where do transient cells stay?
|
Immune system cells--move in and out of connective tissue from the vasiculature
|
|
|
What are the five transient cells?
|
Macrophages, plasma cells, mast cells, lymphocytes, eosinophils
|
|
|
Macrophage:talk about it. What "vessels" are in it?
|
"Big eater" phagocytize any foreign substance (trypan blue is used to see it on a slide, because macrophage phagocytize it)
Also have phagocytic vessels inside it |
|
|
Lymphocytes: talk about it. Where are they abundant? Why? What can they differentiate into?
|
T and by lymphocytes
Fairly inactive Abundant in connective tissue, PARTICULARLY in the GI tract (very open to the outside, so the body will be exposed to a lot of foreign objects, so there's lots of transient molecules there) They can differentiate into PLASMA CELLS, converting quiescent ells into cells ACTIVELY synthesizing protein (immunoglobins) |
|
|
Which are larger, lymphocytes or plasma cells? Where are abundant in plasma cells, and where is the nucleus located? What is special about it?
|
Plasma cells.
Abundant amount of Golgi and ER (characteristic of cells involved with protein synthesis) and nucleus is usually pushed off to one side Nucleus has a cartwheel "clock" fact because of the organization of the heterochromatin (the silent part of the genome), they are very dense and are pushed off to the edge of the nucleus in clumps |
|
|
Mast cells are involved with allergic responses. What is on their surface? What happens when there is an allergic response? What does the mobilization of the cytostolic calcium do? What is released? What do antihistamines do?
|
Have on their surface IgE class antibodies (attached to receptors)
Allergic response: antigen aka allergen crosslinks to IgE antibodies, initiating signaling cascade (including the mobilization of the cytostolic calcium) This mobilization triggers release of granules in the cytoplasm of the mast cells::histamines and proteases and proteoglycans are released Antihistamines: combats release of the histamines::doesn't stop release, just blocks the effects of what is being released |
|
|
What is almost all of the mast cell filled with?
|
Granules (histamines, proteases, proteoglycans, cytokines)
|
|
|
Eosinophils> talk about it. Where is it?
|
Named because they stain a real bright pink with eosin
Found in places where exposure to particular parasites are found (GI) Center is filled with LARGE red staining granules that contain a crystalline center First line of defense in PARASITIC INFECTION Inside it: Eosinophil peroxidase:binds to microorganisms, facilitating their killing my macrophages Major Basic Protein (MBP): major component of crystalline center. binds and disrupts the membrane of parasites Eosinophil cationic protein: together with MBP causes fragmentation of parasites |
|
|
What is the major component of the crystalline center of eosinophil granules? What partners up with it to fragment parasites?
|
Major basic protein
Eosinophil cationic protein works with MBP to fragment |
|
|
What binds to microorganisms facilitating their killing by macrophages in eosinophils?
|
eosinophil peroxidase
|
|
|
What is diapedesis? How does this come about?
|
Circulating lymphocytes move into the connective tissue
Immune cells interact with receptors, proteins on the surface, of endothelial surface called SELECTIN (loose interaction, so they "roll" along the endothelial surface) until, via integrins, a tighter binding occurs and then it is pulled into the cell (diapedesis) and migrates to whatever pulled it in (chemokines) |
|
|
Diabetes: impaired wound healing because of AGE in the connective tissue. Why?
|
Cells are moved to a site of entry: normally, cell is recruited out of vasculature by cytokines to the site of the wound. Transient cells bind with normal ligand in the wound=ENRAGE (endogenous receptor for AGE) and engages to clean up wound to remove the initial collage 3 fibrin clot laid down and allow for the completion of the wound healing
in Diabetics, AGE is found everywhere, including the dermis (and not just the skin injury). It acts like glue, and RAGE (the receptors) immediately engage with the AGE and are activated, as opposed to ENRAGE, so the function of getting to wound is not longer able (does not occur appropriately, occurs adjacent to the vasculature and the underlying connective tissue) Connective tissues will be destroyed down there, and teh fibrin clot area in the injury will not heal, and the wound gets bigger. AGE is what happens with high glucose, engages with RAGE and prevents normal ligand ENRAGE that should occur |
|
|
What is ENRAGE? of ENRAGE, RAGE, and AGE, what is normal to the body, what is the result of diabetes?
|
ENRAGE and RAGE are normal::AGE is the result of high glucose levels
|
