EXAM 3 blood flow atheroschlerosis.txt

• 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

• 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

• 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: 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

• 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

• 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

• 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!

• 1. INCREASE in BLOOD PRESSURE
• 2. INCREASE in OSCILLATION of PRESSURE
• 3. INCREASE in PRO-INFLAMMATORY signaling
• Leads to plaque formation

Not really, it is actually PLA2 activation which causes the pro-inflammatory response