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What's a chylomicron
- lipoproteins and lipids, with FFAs on the outside, chopped of by lipases that interact with the ApoCII enzyme on chylomicron
- HDLs also activated by ApoCII donate fxnl proteins for breakdown of the chylomicron
- Both allow for the transport of the chylomicron out of the blood and into the LIVER!!
- DONATES FXNAL proteins to LDL in order for it to be taken out of the blood stream
- Also picks up cholesterol from tissues and RETURNS to LIVER for BILE Synthesis
Role of lipids
- Absorb fat sol vitamins (ADE&K)
- Synthesize BILE from cholesterol and FFA
- Synthesize STEROID hormones from cholesterol
interacts with ApoCII: allowing it to CHOP of FFAs so it can get outa the blood
Atheroschlerosis occurs at one end of a blood vessel...why?
- Occurs at INSIDE Curvature
- Due to TURBULENT, OSCILLATING Blood Flow
- This causes INTERMITTENT SHEER FORCE, making the CILIA move back and forth, instead of a steady stream
- This Causes Ca channels to OPEN and stay open
Laminar vs oscillating blood flow
- LAMINAR: CONSTANT flow and pressure, with cilia all curved in one direction, so Ca channels are CLOSED, sometimes cilia disappears
- OSCILLATING (TURBULENT) sheer force: results in changes pressure, fluctuating BLOOD PRESSURE. Also cilia move back and forth, and this causes Ca channels to open
RESULT of laminar vs oscillating blood flow on blood vessel
- laminar: NO pro-inflammatory response, no channels open, so similar to resolvin (an anti-inflammatory)
- OSCILLATING SHeer force: Increase in signaling, Ca open channels allow for more signals, Phospholipase A2 signaling activation, causing clipping of AAs, which then aids in production of pro-inflammatory (prost, leuk, throm).
- With ILs and TNF CONTINUALLY ACTIVATED..with the stressor present, they help Monocytes MOVE TOWARDS IL-increased concentrations
**Basic sequence with intermittent turbulent flow (Oscillating sheer force)
- cilia back and forth due to pressure changes, causing fluctuation in blood pressure
- increase Ca channels due to this
- increase signaling, activation of PLA2, chopping AAs to generate pro-inflammatory pros, throm, leuk
- increase in ILs and TNF with the continued stress present
- increases monocyte movement towards this area (where ILs are)
- increased MACROPHAGE activity in this region..producing MORE RADICALS
**Activated Macrophages cause what?
- Macrophages that are activated cause activation of NAD OXIDASE enzyme on its surface
- These NADs produce superoxides...and result is MORE OXIDATIVE DAMAGE!
- Macrophages that get too big (too much lipid content) also cannot go to the LYMPH, where they should, so they are stuck in the blood!
How does Plaque form, in three steps
- 1. INCREASE in BLOOD PRESSURE
- 2. INCREASE in OSCILLATION of PRESSURE
- 3. INCREASE in PRO-INFLAMMATORY signaling
- Leads to plaque formation
Is AA pro-inflammatory?
Not really, it is actually PLA2 activation which causes the pro-inflammatory response